DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCEICRP ref 4838-4528-4881
20 September 2012

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Annals of the ICRP

8910ICRP PUBLICATION XXX

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Occupational Intakes of Radionuclides
Part 3

DRAFT DOCUMENT
Information in this consultation document is preliminary. The document should not be cited in any published material inadvance of final approval for publication by the Commission of ICRP.

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Occupational Intakes of Radionuclides
Part 345
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ICRP Publication XXX

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Approved by the Commission in XXX

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Abstract- The 2007 Recommendations (Publication 103, ICRP, 2007) introduced changes tothe radiation and tissue weighting factors used in calculation of effective dose. In addition,
Publication 103 clarified the need for separate calculation of equivalent dose to males andfemales and sex-averaging in the calculation of effective dose (ICRP, 2007) and adopted theuse of reference anatomical computational phantoms, in place of the composite mathematicalmodels that have been used previously.
These substantial changes implied a revision of the dose coefficients for internal exposure,published previously in the Publication 30 series (ICRP, 1979, 1980, 1981, 1988b). This
work was performed by Committee 2 and its Task Groups INDOS and DOCAL.
This report is the third in a series of documents replacing the Publication 30 series andPublication 68 (ICRP, 1994b) and providing revised dose coefficients for occupational
intakes of radionuclides (OIR) by inhalation and ingestion. It provides data on individual
elements and their radioisotopes, including biokinetic data and models, dose coefficients anddata for bioassay interpretation. Electronic disks accompanying this series give extensive
additional information.
This third report in the series provides the above data for the following elements :Ruthenium (Ru), Antimony (Sb), Tellurium (Te), Iodine (I), Caesium (Cs), Barium (Ba),
Iridium (Ir), Lead (Pb), Bismuth (Bi), Polonium (Po), Radon (Rn), Radium (Ra), Thorium(Th) and Uranium (U).
The current version, posted for public consultation, contains only the biokinetic data andthe models. An exception is made for Radon, where some preliminary dose coeffcients areprovided for information only.
The total set of dose coefficients and data for bioassay interpretation will be included in
the final version.
© 201X ICRP. Published by Elsevier Ltd.
Keywords: Occupational exposure, Internal Dose Assessment, Biokinetic and Dosimetricmodels, Bioassays interpretation.

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CONTENTS

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PREFACE .................................................................................................................................. 783

1. INTRODUCTION ............................................................................................................... 9

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2. RUTHENIUM (Z = 44) ..................................................................................................... 122.1. CHEMICAL FORMS IN THE WORKPLACE ........................................................................ 122.2. ROUTES OF INTAKE ..................................................................................................... 122.2.1. INHALATION ........................................................................................................ 122.2.2. INGESTION ........................................................................................................... 19
2.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION ...................................... 20
2.2.3.1. Summary of the database ............................................................................ 20
2.2.3.2. Biokinetic model for systemic ruthenium ................................................... 22
2.2.3.3. Treatment of radioactive progeny ............................................................... 25
2.3. INDIVIDUAL MONITORING ............................................................................................ 26

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3. ANTIMONY (Z = 51) ....................................................................................................... 29
3.1. CHEMICAL FORMS IN THE WORKPLACE....................................................................... 29
3.2. ROUTES OF INTAKE ..................................................................................................... 29
3.2.1. INHALATION ........................................................................................................ 29
3.2.2. INGESTION ........................................................................................................... 32
3.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION ...................................... 33
3.2.3.1. Summary of the database ............................................................................ 33
3.2.3.2. Biokinetic model for systemic antimony .................................................... 38
3.2.3.3. Treatment of radioactive progeny ............................................................... 41
3.3. INDIVIDUAL MONITORING ............................................................................................ 42

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4. TELLURIUM (Z = 52) ...................................................................................................... 46
4.1. CHEMICAL FORMS IN THE WORKPLACE....................................................................... 46
4.2. ROUTES OF INTAKE ..................................................................................................... 46
4.2.1. INHALATION ........................................................................................................ 46
4.2.2. INGESTION ........................................................................................................... 49
4.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION ...................................... 50
4.2.3.1. Summary of the database ............................................................................ 50
4.2.3.2. Biokinetic model for systemic tellurium ..................................................... 54
4.2.3.3. Treatment of radioactive progeny ............................................................... 56
4.3. INDIVIDUAL MONITORING ............................................................................................ 58

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5. IODINE (Z = 53) ............................................................................................................... 61
5.1. CHEMICAL FORMS IN THE WORKPLACE....................................................................... 61
5.2. ROUTES OF INTAKE ..................................................................................................... 61
5.2.1. INHALATION ........................................................................................................ 61
5.2.2. INGESTION ........................................................................................................... 65
5.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION ...................................... 66
5.2.3.1. Summary of the database ............................................................................ 66
5.2.3.2. Biokinetic model for systemic iodine ......................................................... 72
5.2.3.3. Treatment of radioactive progeny ............................................................... 793

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5.3. INDIVIDUAL MONITORING ............................................................................................ 80

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6. CAESIUM (Z = 55) ........................................................................................................... 90
6.1. CHEMICAL FORMS IN THE WORKPLACE....................................................................... 90
6.2. ROUTES OF INTAKE ..................................................................................................... 90
6.2.1. INHALATION ........................................................................................................ 90
6.2.2. INGESTION ........................................................................................................... 94
6.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION ...................................... 95
6.2.3.1. Summary of database .................................................................................. 95
6.2.3.2. Biokinetic model for systemic caesium ...................................................... 96
6.2.3.3. Treatment of radioactive progeny ............................................................. 102
6.2.3.4. Differences with gender ............................................................................ 104
6.3. INDIVIDUAL MONITORING .......................................................................................... 104

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7. BARIUM (Z = 56) ........................................................................................................... 110
7.1. CHEMICAL FORMS IN THE WORKPLACE..................................................................... 110
7.2. ROUTES OF INTAKE ................................................................................................... 110
7.2.1. INHALATION ...................................................................................................... 110
7.2.2. INGESTION ......................................................................................................... 113
7.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .................................... 114
7.2.3.1. Summary of the database .......................................................................... 114
7.2.3.2. Biokinetic model for systemic barium ...................................................... 114
7.2.3.3. Treatment of radioactive progeny ............................................................. 119
7.3. INDIVIDUAL MONITORING .......................................................................................... 119

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8. IRIDIUM (Z = 77) ........................................................................................................... 123
8.1. CHEMICAL FORMS IN THE WORKPLACE..................................................................... 123
8.2. ROUTES OF INTAKE ................................................................................................... 123
8.2.1. INHALATION ...................................................................................................... 123
8.2.2. INGESTION ......................................................................................................... 126
8.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .................................... 126
8.2.3.1. Summary of the database .......................................................................... 126
8.2.3.2. Biokinetic model for systemic iridium ...................................................... 128
8.2.3.3. Treatment of radioactive progeny ............................................................. 131
8.3. INDIVIDUAL MONITORING .......................................................................................... 133

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9. LEAD (Z = 82) ................................................................................................................ 136
9.1. CHEMICAL FORMS IN THE WORKPLACE..................................................................... 136
9.2. ROUTES OF INTAKE ................................................................................................... 136
9.2.1. INHALATION ...................................................................................................... 136
9.2.2. INGESTION ......................................................................................................... 149
9.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .................................... 150
9.2.3.1. Summary of the database .......................................................................... 150
9.2.3.2. Biokinetic model for systemic lead ........................................................... 152
9.2.3.3. Treatment of radioactive progeny ............................................................. 155
9.3. INDIVIDUAL MONITORING .......................................................................................... 159

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10. BISMUTH (Z = 83) ....................................................................................................... 167

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10.1. CHEMICAL FORMS IN THE WORKPLACE .................................................................... 167
10.2. ROUTES OF INTAKE.................................................................................................. 167
10.2.1. INHALATION..................................................................................................... 167
10.2.2. INGESTION ....................................................................................................... 172
10.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .................................. 173
10.2.3.1. Summary of the database ........................................................................ 173
10.2.3.2. Systemic model ....................................................................................... 176
10.2.3.3. Treatment of radioactive progeny ........................................................... 178
10.3. INDIVIDUAL MONITORING ........................................................................................ 178

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11. POLONIUM (Z = 84) .................................................................................................... 182
11.1. CHEMICAL FORMS IN THE WORKPLACE .................................................................... 182
11.2. ROUTES OF INTAKE.................................................................................................. 182
11.2.1. INHALATION..................................................................................................... 182
11.2.2. INGESTION ....................................................................................................... 191
11.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .................................. 191
11.2.3.1. Summary of the database ........................................................................ 191
11.2.3.2. Biokinetic model for systemic polonium ................................................ 194
11.2.3.3. Treatment of radioactive progeny ........................................................... 199
11.3. INDIVIDUAL MONITORING ........................................................................................ 200

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12. RADON (Z = 86) ........................................................................................................... 204
12.1. CHEMICAL FORMS IN THE WORKPLACE .................................................................... 204
12.2. SPECIAL QUANTITIES AND UNITS.............................................................................. 207
12.3. EXTERNAL DOSE...................................................................................................... 210
12.4. ROUTES OF INTAKE.................................................................................................. 210
12.4.1. INHALATION..................................................................................................... 210
12.4.2. INGESTION ....................................................................................................... 224
12.4.3. BIOKINETIC MODEL FOR RADON GAS ................................................................ 224
12.4.3.1. Summary of the database ........................................................................ 225
12.4.3.2. Biokinetic model for systemic radon....................................................... 228
12.4.3.3. Treatment of radioactive progeny ........................................................... 232
12.5. DOSIMETRY ............................................................................................................. 235
12.5.1. CALCULATION OF DOSE CONVERSION FACTOR ARISING FROM THE INHALATION OF
RADON PROGENY..................................................................................................................... 235
12.5.2. INHALATION OF RADON GAS ............................................................................. 238
12.5.3. INGESTION OF RADON....................................................................................... 238
12.5.4. USE OF DOSE COEFFICIENTS FOR RADON-222 AND RADON-220 AND THEIR SHORTLIVED DECAY PRODUCTS ......................................................................................................... 238

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13. RADIUM (Z = 88) ......................................................................................................... 246
13.1. CHEMICAL FORMS IN THE WORKPLACE ................................................................... 246
13.2. ROUTES OF INTAKE.................................................................................................. 246
13.2.1. INHALATION..................................................................................................... 246
13.2.2. INGESTION ....................................................................................................... 249
13.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .................................. 250
13.2.3.1. Biokinetic database ................................................................................. 250
13.2.3.2. Biokinetic model for systemic radium .................................................... 250

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13.2.3.3. Treatment of radioactive progeny ........................................................... 254
13.3. INDIVIDUAL MONITORING ....................................................................................... 258

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14. THORIUM (Z = 90) ....................................................................................................... 262
14.1. CHEMICAL FORMS IN THE WORKPLACE ................................................................... 262
14.2. ROUTES OF INTAKE.................................................................................................. 262
14.2.1. INHALATION..................................................................................................... 262
14.2.2. INGESTION ....................................................................................................... 276
14.2.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION ................................... 277
14.2.3.1. Summary of the database ........................................................................ 277
14.2.3.2. Biokinetic model for systemic thorium ................................................... 279
14.2.3.3. Treatment of radioactive progeny ........................................................... 282
14.3. INDIVIDUAL MONITORING ........................................................................................ 283

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15. URANIUM (Z = 92) ...................................................................................................... 290
15.1. CHEMICAL FORMS IN THE WORKPLACE .................................................................... 290
15.2. ROUTES OF INTAKE.................................................................................................. 290
15.2.1. INHALATION..................................................................................................... 290
15.2.2. INGESTION ....................................................................................................... 303
15.3. SYSTEMIC DISTRIBUTION, RETENTION AND EXCRETION .......................................... 304
15.3.1. SUMMARY OF THE DATABASE .......................................................................... 304
15.3.2. BIOKINETIC MODEL FOR SYSTEMIC URANIUM ................................................... 307
15.3.3. TREATMENT OF RADIOACTIVE PROGENY .......................................................... 312
15.4. INDIVIDUAL MONITORING ........................................................................................ 313

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PREFACE

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The 2007 Recommendations (Publication 103, ICRP, 2007) introduced changes to theradiation weighting factors used in the calculation of equivalent dose to organs and tissues
and also changes to the tissue weighting factors used in the calculation of effective dose. In
addition, an important development was the adoption of reference anatomical computational
phantoms, in place of the composite mathematical models that have been used for all
previous calculations of organ doses. Publication 103 also clarified the need for separate
calculation of equivalent dose to males and females and sex-averaging in the calculation ofeffective dose (ICRP, 2007).
These changes implied a revision of the dose coefficients initially provided in the
Publication 30 series (ICRP, 1979, 1980, 1981, 1988b). This work was performed byCommittee 2 and its Task Groups INDOS and DOCAL.
This report is the third in a series of documents replacing the Publication 30 series andPublication 68 (ICRP, 1994b) and providing revised dose coefficients for occupational
intakes of radionuclides (OIR) by inhalation and ingestion. It provides also radionuclidespecific information for the design and planning of monitoring programmes and retrospective
assessment of occupational internal doses, replacing Publications 54 and 78 (ICRP, 1988a,
1997b).
The first report of this OIR series included chapters describing the control of occupational
exposures, biokinetic and dosimetric models, monitoring methods, monitoring programmes
and retrospective dose assessment.
The following reports provide data on individual elements and their radioisotopes,
including biokinetic data and models, dose coefficients and data for bioassay interpretation.
Electronic disks accompanying this series give extensive additional information.
The second report in the series provided data for the following elements : Hydrogen (H),
Carbon (C), Phosphorus (P), Sulphur (S), Calcium (Ca), Iron (Fe), Cobalt (Co), Zinc (Zn),
Strontium (Sr), Yttrium (Y), Zirconium (Zr), Niobium (Nb), Molybdenum (Mo) andTechnetium (Tc).
This third report provides the data for the following elements: Ruthenium (Ru), Antimony(Sb), Tellurium (Te), Iodine (I), Caesium (Cs), Barium (Ba), Iridium (Ir), Lead (Pb), Bismuth(Bi), Polonium (Po), Radon (Rn), Radium (Ra), Thorium (Th) and Uranium (U).
Subsequent reports will provide data for the other elements.
The current version, posted for public consultation, contains only the biokinetic data andthe models. An exception is made for Radon, where some preliminary dose coeffcients areprovided for information only.
The total set of dose coefficients and data for bioassay interpretation will be included in
the final version.
The membership of the Task Group on Internal Dosimetry (INDOS) at the time of thecompletion of this report was:Members:
F Paquet (Chair)
E Ansoborlo
M R Bailey

G Etherington
A Giussani
R A Guilmette

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J L Lipsztein
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E J A Blanchardon
H Doerfel

J D Harrison
R W Leggett

Corresponding Members:
A Bouville
C-M Castellani
R Cruz-Suarez
C Hurtgen

A Luciani
D Newton
D Nosske
D M Taylor

D Whillans

The membership of the Task Group on Dose Calculations (DOCAL) at the time of thecompletion of this report was:Members:W E Bolch (Chair)
M Zankl
D Nosske
N Petoussi-Henss
M Pelliccioni
Corresponding Members:
A Birchall
G Gualdrini
D Jokisch
C Lee

A EndoV Berkovski
L Bertelli
K F Eckerman

N Ishigure
T P FellN E Hertel
J G S Hunt

H Schlattl
M Stabin
R Tanner
X G XuThe membership of Committee 2 was:(2009-2013)
H-G Menzel (Chair)
F Paquet
N Ishigure
G Dietze
D Bartlett
V Berkovski

W E Bolch
M R Bailey
N Petoussi-Henss
R W Leggett
K F Eckerman
A Endo8

J D Harrison
R Cox
M BalonovA S Pradhan
J L Lipsztein
J Ma

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1.

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INTRODUCTION(1)
The present report is Part 3 of a report series aimed at providing revised dosecoefficients for occupational intakes of radionuclides (OIR) by inhalation and ingestion. It
also presents radionuclide-specific information for the design and planning of monitoring
programmes and retrospective assessment of occupational internal doses.
(2)This report series replaces the Publication 30 series (ICRP, 1979, 1980, 1981,
1988b), Publications 54, 68 and 78 (ICRP, 1988a, 1994b, 1997). The revised dosecoefficients, dose per unit content values and reference bioassay functions have been
calculated using the Publication 100 (ICRP, 2006) Human Alimentary Tract Model (HATM)
and a revision of the Publication 66 (ICRP, 1994a) Human Respiratory Tract Model (HRTM)
which takes account of more recent data. The revisions made to the HRTM are described inPart 1 of this report series. In addition, information is provided in this report series on
absorption to blood following inhalation and ingestion of different chemical forms ofelements and their radioisotopes, in those cases for which it is currently judged that the data
are sufficient to make specific recommendations. Revisions have been made to many models
for the systemic biokinetics of radionuclides, making them more physiologically realistic
representations of uptake and retention in organs and tissues and of excretion.
(3)
The dose coefficients and dose per unit content values presented in this report series
1 are given for a Reference Worker with an average breathing rate of 1.2 m3 h-1 during an 8 hworking day. These data are provided for a range of physico-chemical forms for eachradionuclide and for a range of aerosol particle size distributions. Data for ingestion andinjection (i.e. direct entry to the blood) are provided to allow the interpretation of bioassay
data for cases of inadvertent ingestion (e.g. of material on contaminated skin) or rapid
absorption through intact or damaged skin (injection).
(4)
Data are presented in a standard format for each element and its radioisotopes. Eachelement section provides information on chemical forms encountered in the workplace;principal radioisotopes, their physical half-lives and decay modes; reviews of data on
inhalation, ingestion and systemic biokinetics; the structure and parameter values for thesystemic biokinetic model; and information on the interpretation of individual monitoringdata. Each section in the printed documents also includes tables of:

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•

Dose coefficients (committed effective dose, Sv, per Bq intake) for inhalation of 5µm AMAD aerosols with the default absorption Types appropriate for theelement, for all relevant radioisotopes;•

Principal emissions of selected radioisotopes;•

Measurement techniques, detection limits typically achieved in a practicalmonitoring programme, and improved detection limits that could be achieved bysuitable choice of measurement parameter values, for selected radioisotopes;•

Committed effective dose (Sv) per unit measurement (Bq) for an acute intake byinhalation of a 5 µm AMAD aerosol with the default absorption Types appropriate

1

The current version, posted for public consultation, contains only the biokinetic data and the models. An
exception is made for Radon, where some preliminary dose coeffcients are provided for information only.
The total set of dose coefficients and data for bioassay interpretation will be included in the final version

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for the element, for selected radioisotopes;

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Bioassay data (i.e. whole body and/or organ retention, and daily urinary and faecal
excretion, Bq per Bq intake), at various times after an acute intake by inhalation ofa 5 µm AMAD aerosol with the default absorption Types appropriate for theelement;(5)
Bioassay data are also presented graphically.
(6)
In cases for which sufficient information is available (principally for actinide
elements), lung absorption is specified for different chemical forms and dose coefficients andbioassay data are calculated accordingly.
(7)
The full data set of this report is provided on electronic disk. This disk contains inaddition to the printed document:
Dose coefficients• Committed equivalent dose coefficients for organs and tissues, for males andfemales;•

Dose coefficients for all chemical forms considered;•

Dose coefficients for an inhaled aerosol with particle sizes ranging from an
AMTD of 0.001 µm to an AMAD of 20 µm;•

Dose coefficients for intake by ingestion, with the default fA values appropriate forthe element, for all relevant radioisotopes;•

Dose coefficients for radioisotopes not given in the printed reports in this series.

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Bioassay data•

Committed effective dose (Sv) per unit measurement (Bq) for an acute intake byinhalation of an aerosol with particle sizes ranging from an AMTD of 0.001 µm to
an AMAD of 20 µm;•

Committed effective dose (Sv) per unit measurement (Bq) for an acute intake byingestion, with default fA values appropriate for the element;•

Bioassay data (i.e. whole body and/or organ retention, and daily urinary and faecal
excretion, Bq per Bq intake), for an acute intake by inhalation of an aerosol withparticle sizes ranging from an AMTD of 0.001 µm to an AMAD of 20 µm;•

Similar bioassay data for an acute intake by ingestion•

Figures giving measured activity content per unit dose (Bq Sv–1) in selected bodytissues, urine (daily excretion) or faeces (daily excretion), at various times after
intake by inhalation or ingestion. These data can also be used to facilitate
decisions about the design of monitoring programmes and the extent of theassessment required, as described in Chapter 5 of OIR Part 1.

(8)
The list of elements included in Part 3 is: Ruthenium (Ru), Antimony (Sb),
Tellurium (Te), Iodine (I), Caesium (Cs), Barium (Ba), Iridium (Ir), Lead (Pb), Bismuth (Bi),10

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Polonium (Po), Radon (Rn), Radium (Ra), Thorium (Th) and Uranium (U).
References
ICRP, 1979. Limits for intake of radionuclides by workers. ICRP Publication 30, Part 1. Ann. ICRP
2(3/4).
ICRP, 1980. Limits for intakes of radionuclides by workers. ICRP Publication 30, Part 2. Ann. ICRP
4(3/4).
ICRP, 1981. Limits for intakes of radionuclides by workers. ICRP Publication 30, Part 3. Ann. ICRP
6 (2/3).
ICRP, 1988a. Individual monitoring for intakes of radionuclides by workers: design andinterpretation. ICRP Publication 54, Ann. ICRP 19 (1-3).
ICRP, 1988b. Limits for intakes of radionuclides by workers: An Addendum. ICRP Publication 30,
Part 4. Ann. ICRP 19 (4).
ICRP, 1994a. Human respiratory tract model for radiological protection. ICRP Publication 66. Ann.
ICRP 24 (1-3).
ICRP, 1994b. Dose coefficients for intake of radionuclides by workers. ICRP Publication 68. Ann.
ICRP 24 (4).
ICRP, 1997. Individual monitoring for internal exposure of workers – Replacement of ICRP
Publication 54. ICRP Publication 78. Ann. ICRP 27 (3/4).
ICRP, 2006. Human alimentary tract model for radiological protection. ICRP Publication 100. Ann.
ICRP 36 (1-2).
ICRP, 2007. The 2007 Recommendations of the International Commission on RadiologicalProtection. ICRP Publication 103. Ann. ICRP 37 (2-4).

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2.

2.1. Chemical forms in the workplace(9)
Ruthenium is a transition metal which may exist in various oxidation states from II
to VIII. It is assumed that oxidation states (III) and (IV) are the most stable, while in strongly
oxidation conditions the oxo-anion RuO42- is very stable. Ruthenium may be encountered inindustry in a variety of chemical and physical forms, such as oxides (RuO2 and RuO4 (vapour
state)), halides, sulphides and different cyanides.
(10) Ruthenium-103 is produced in the nuclear industry as a fission product. At the
Chernobyl accident, ruthenium became volatile during the fire and was found in metallic
form, hundreds of kilometres away from the plant (Pollanen, 1997).
Table 2-1. Isotopes of ruthenium addressed in this report
Isotope
Ru-94
Ru-95
Ru-97
Ru-103
Ru-105
Ru-106a

443
444
445
446
447
448
449
450
451
452
453
454
455
456
457
458
459
460
461
462
463
464
465
466
467
468

RUTHENIUM (Z = 44)aPhysical half-life
51.8 m1.643 h2.9 d39.26 d4.44 h373.59 d

Decay mode
EC, B+
EC, B+EC
BBB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

2.2.

Routes of Intake

2.2.1. Inhalation
Absorption Types and parameter values(11) Some information is available on the behaviour of inhaled ruthenium in man
following accidental intakes as an oxide or in irradiated fuel fragments. Information isavailable from experimental studies of ruthenium as tetroxide, chloride, citrate, dioxide, andirradiated uranium dioxide.
(12) Absorption parameter values and Types, and associated fA values for gas and vapour
forms of ruthenium are given in Table 2-2 and for particulate forms in Table 2-3. Exposures
to gas and vapour forms of ruthenium are relatively unusual compared to exposures toparticulate forms, and therefore it is proposed here that particulate form is assumed in theabsence of information (ICRP, 2002).
Gases and vapours
Ruthenium tetroxide (RuO4)(13) Ruthenium tetroxide (melting point 26°C, boiling point 40°C) has a high vapour
pressure at room temperature and is thought to have been involved in several humaninhalation incidents (Snipes and Kanapilly, 1983). It is very reactive, and converts toruthenium dioxide in contact with organic or other reactive surfaces.
(14) Snipes et al. (1977) carried out pilot experiments in which the biokinetics of 103Ru

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were followed for ~2 weeks after inhalation of 103RuO4 by dogs and rats. In both species
initial deposition was primarily in the nasopharyngeal region (NP, broadly equivalent to theextrathoracic airways) and tracheobronchial region (TB, equivalent to the bronchial andbronchiolar regions). Clearance was rapid and mainly fecal: ~85% of the initial body burden(IBB) was retained with a half-time of ~1 day, and the rest with a half-time of ~1 week. At
the end of the study most of the 103Ru retained in the body in dogs was in the lungs, but in rats
was associated with the nasal turbinates.
(15) Runkle et al. (1980) followed the biokinetics of 106Ru for 112 days after inhalation of
106
RuO4 by rats. Complementary experiments were conducted to measure absorption of 106Ru
following gavage of 106RuO4 or 106RuO2: fractional absorption was estimated to be ~0.01 forboth. The overall pattern following inhalation was similar to that observed by Snipes et al.
(1977): 85%, 13.8% and 1.2% IBB were retained with biological half-times of 0.6, 4 and 69
days, respectively. Initial deposition was mainly in the NP and TB regions. After the firstweek most of the 106Ru retained was associated with the nasal turbinates and head skin, withlittle systemic uptake. Although most of the 106Ru deposited in the turbinates cleared within a
few days, ~2% was retained with a half-time of ~70 days. As discussed below, bound stateparameter values for ruthenium of fb = 0.05 and sb = 0.1 d–1 were chosen here. Assumingthese values, dissolution parameter values fitted here for 106RuO4 inhaled by rats (withregional deposition of 99.8% ET and 0.2% AI) were: fr = 0.92, sr = 0.35 d–1 and ss = 0.01 d–1.
(16) Snipes (1981) followed the biokinetics of 106Ru for 512 days after inhalation of
106
RuO4 by dogs. In a complementary experiment the biokinetics of 106Ru were followed for 5days after ingestion of 106RuO2 by dogs: fractional absorption was estimated to be ~0.005.
The overall pattern after inhalation was similar to that observed by Snipes et al. (1977), but
clearance was even faster: 90%, 0.7% and 0.3% IBB were retained with effective half-timesof 1.2, 14 and 170 days, respectively. Again, initial deposition was primarily in the NP and
TB regions. The respiratory tract and pelt contained the highest levels of 106Ru with relatively
little systemic uptake. The NP region contained a high proportion of the body content of
106
Ru at all times. The trachea, larynx and lung contained similar amounts of 106Ru at 512
days after exposure, reflecting long-term retention of some of the initial deposit in all regionsof the respiratory tract. Autoradiographs showed that the 106Ru dispersion in the turbinates
and lymph nodes was relatively uniform: only single tracks were observed with no indicationsof focal accumulation. The long-term retention of a fraction of the 106Ru in the conducting
airways, from which most particles are cleared rapidly, and the uniform dispersion shown in
the autoradiographs, provide strong evidence for a bound fraction for ruthenium. Based on
the results of this study, bound state parameter values for ruthenium of fb = 0.05 andsb = 0.1 d–1 were chosen here. Assuming these values, dissolution parameter values fitted
here for 106RuO4 inhaled by dogs (with regional deposition of 35% ET1; 35% ET2; 17% BB
and 0.02% AI) were: fr = 0.4, sr = 10 d–1 and ss = 0.001 d–1.
(17) Snipes and Kanapilly (1983) pointed out that incidents involving a release of RuO4
into room air might produce complex exposure atmospheres, with components including
RuO4 vapour, ultrafine particles formed by self-nucleation of RuO2, molecular RuO4 or RuO2
adsorbed on or attached to particles in the air. Such complex mixtures of vapour and particles
could yield deposition and dose patterns different from those of RuO4 vapour or of a simple
particulate aerosol. To provide data to assist in assessing doses from such exposures, Snipes
and Kanapilly (1983) followed the biokinetics of 106Ru for 112 days after inhalation by rats of106
RuO4 mixed with an aerosol of fused aluminosilicate particles (FAP, 0.69 µm diameter.)Particle size analysis and the initial deposition pattern indicated that most of the 106Ru in the
exposure chamber was in the form of molecular RuO4, with ~25% associated with particles
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~0.1 µm diameter, and <5% associated with the FAP. It was estimated that 60% IBB
deposited in the upper respiratory tract, 10% in the TB region, 12% in the AI region and 18%
was external contamination, mainly on the nares and head skin. Clearance was rapid andmainly via the alimentary tract to faeces: 92% and 8% IBB were retained with effective halftimes of 0.7 and 30 days, respectively. Clearance of 106Ru from the AI region had an effective
half-time of ~30 days and was predominantly by dissolution. As discussed below, bound stateparameter values for ruthenium of fb = 0.05 and sb = 0.1 d–1 were chosen here. Assumingthese values, dissolution parameter values fitted here (with regional deposition of 87% ET2
and 13% AI) were: fr = 0.9, sr = 0.5 d–1 and ss = 0.001 d–1. These are similar to those assessed
for RuO4 alone. The main difference is in the higher lung deposition.
(18) A worker accidentally inhaled 103RuO4 vapour while performing experiments inwhich 103Ru was distilled from a neutron-irradiated 235U sample (Webber and Harvey, 1976).
External measurements made from 8 to 36 days after the incident indicated that inhaledactivity was retained primarily in the region of the nose and mouth. Activity was also detectedin the lower abdominal area. There was no evidence of concentration of activity in othertissues. The half-time for biological removal from the body was ~15 d. There is insufficient
information available to assess parameter values from the reported measurements, but theobservations are consistent with parameter values fr = 0.4 and ss = 0.001 d–1 derived abovefrom experimental studies.
(19) In two other human exposure incidents (Pusch 1968; Howells et al., 1977) it wassuspected that the released activity was RuO4, but that it was converted at least in part toparticulate forms of ruthenium, notably RuO2, during mixing and interacting with room air(Snipes and Kanapilly, 1983). In both cases the ruthenium was only detected in the chest.
Details are given below in the ruthenium dioxide section.
(20) Based on the experimental studies, dissolution parameter values used here for RuO4
are: fr = 0.5, sr = 1 d–1 and ss = 0.001 d–1, with bound state parameter values for ruthenium of
fb = 0.05 and sb = 0.1 d–1 (consistent with assignment to default Type M) and fA = 0.01.
Regional deposition of 40% ET1; 40% ET2; 12% BB; 7% bb and 1% AI is assumed here,
based on 106RuO4 inhaled by dogs.
(21) However, the study by Snipes and Kanapilly (1983) and the accidental exposuressuggest that mixing with the ambient aerosol could lead to greater lung deposition of RuO4
and conversion to RuO2 before intake. For prospective assessments of potential releases of
RuO4 it is therefore proposed that the exposure is to 50% RuO4 vapour and 50% RuO2
particulate (5 µm AMAD aerosol). For retrospective assessment it should be recognised that awide range of mixtures is possible.
Particulate aerosols
Ruthenium chloride(22) Thompson et al. (1958) measured excretion of 106Ru for 60 days after administrationof ruthenium chloride to rats by intratracheal instillation, and the tissue distribution at the endof the experiment. They estimated that cumulative urinary excretion accounted for ~29% of
the initial lung deposit (ILD), cumulative faecal excretion ~66%, activity in the respiratory
tract ~2%, and activity in systemic tissues ~3% of the administered amount. Excretion in
faeces exceeded that in urine for about 15 days, and was much higher than following
intravenous or intraperitoneal injection. This suggests that much of the activity deposited in
the lung was cleared by particle transport to the alimentary tract before it could be absorbed,
i.e. that sr <100 d–1. However, ~10% ILD was excreted in urine in the first few days,
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suggesting that sr >1 d–1.
(23) Burykina (1969) followed the lung retention of 106Ru for 75 days after administrationof ruthenium chloride to rats by intratracheal instillation. Although there was some rapid
clearance from the lungs ~10% ILD remained in the lungs at 75 d. As discussed below, boundstate parameter values for ruthenium of fb = 0.05 and sb = 0.1 d–1 are used here. Assumingthese values, dissolution parameter values fitted here were: fr = 0.8, sr = 4 d-1 and ss = 0.007 d–
1, consistent with assignment to Type M.
(24) Dobryakova (1970) followed the biokinetics of 106Ru for 14 days after administrationof ruthenium chloride to rats by intratracheal instillation. There was rapid absorption from thelungs: ~50% of the ILD was absorbed at 30 minutes and ~70% ILD at 1 day. Subsequent
clearance was slower and excretion mainly faecal, with ~6% ILD remaining in the lungs at 14d. As discussed below, bound state parameter values for ruthenium of fb = 0.05 and sb = 0.1 d–
1
are used here. Assuming these values, dissolution parameter values fitted here were: fr =0.8, sr = 10 d–1 and ss = 0.1 d–1, consistent with assignment to Type F.
(25) Although specific parameter values for ruthenium chloride based on in vivo data are
available, they are not adopted here, because inhalation exposure to it is unlikely. Instead,ruthenium chloride is assigned to Type F.
Ruthenium oxalate(26) Newton and Latven (1971) followed the biokinetics of 106Ru for 16 days after
inhalation by a dog of 106Ru oxalate, heat-treated at 100°C. (Other dogs inhaled 106Ru oxalate
aerosols heat-treated at 500°C or 1000°C, which was thought to convert most of the 106Ru to
106
RuO2: see below). In a complementary experiment fractional absorption of 106Ru from thealimentary tract after administration of the same material by gavage to a dog was estimated tobe ~0.2. Following inhalation, clearance was rapid: 73% IBB was excreted in the first 4 days,
and the rest with a half-time of 14 days. At 16 days, 40% of the retained 103Ru was in thelungs, (~10% ILD) suggesting either Type F or Type M behaviour. The rest was widelydistributed. However, 4% was associated with the nasal turbinates: a much larger fraction
than after inhalation of particles treated at higher temperatures (~0.1%), and suggesting
retention of a bound fraction.
(27) Newton et al. (1975, 1976) followed the biokinetics of 106Ru for 365 days after
inhalation by hamsters of 106Ru oxalate aerosols heat-treated at 27°C, 300°C, 600°C or
1100°C. It was considered that at 27°C and 300°C mixed aerosols were formed whichcontained ruthenium oxalate and degradation products, but at 600°C or 1100°C most of the106
Ru was converted to 106RuO2: see below. In dissolution tests in vitro (synthetic serum
ultrafiltrate at 37°C) ~38% and ~33% dissolved from aerosol samples formed at 27°C and
300°C, respectively, mainly in the first day, suggesting fr ~0.3, and sr >10 d–1. At 8 days after
inhalation of aerosol formed at 27°C, ~30% of the retained 106Ru was in the lungs, with ~5%in the skeleton and ~20% in soft tissues. For the particles formed at 300°C, lung retention was
somewhat higher and systemic uptake lower. For both aerosols, ~7% was in the skull, andwas attributed to retention of 106Ru in the NP region. As discussed below, bound stateparameter values for ruthenium of fb = 0.05 and sb = 0.1 d–1 are used here. Assuming thesevalues, dissolution parameter values fitted here for the aerosol formed at 27°C were: fr = 0.36,
sr = 37 d–1 and ss = 0.1 d–1, consistent with assignment to Type F; and for the aerosol formed
at 300°C, fr = 0.28, sr = 34 d–1 and ss = 0.008 d–1, consistent with assignment to Type M.
(28) Although specific parameter values for ruthenium oxalate based on in vivo data are
available, they are not adopted here, because inhalation exposure to it is unlikely. Instead,ruthenium oxalate is assigned to Type F.
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Ruthenium citrate(29) Boecker and Harris (1969) followed the biokinetics of 106Ru for 512 days after
inhalation of 106Ru citrate by dogs. Whole-body retention was represented by a fourcomponent exponential function: 80%, 13%, 4% and 3% IBB were retained with effective
half-times of 0.6, 11, 53 and 280 days, respectively. The large amounts excreted in the firstfew days, in both urine and faeces, suggest that much of the activity deposited in the
respiratory tract was absorbed rapidly, at a rate similar to particle transport from the upper
airways to the alimentary tract. Subsequent excretion was mainly to urine. Soon after
exposure, the lungs contained about 40% IBB, and this decreased to ~4% IBB after 16 days.
There was wide distribution of the 106Ru retained in the body, but the concentration in lungs
remained higher than in other tissues. The authors suggested that hydrolysis of the polyvalentruthenium might have caused the long-term lung retention. As discussed below, bound stateparameter values for ruthenium of fb = 0.05 and sb = 0.1 d–1 are used here. Assuming thesevalues, dissolution parameter values fitted here were: fr = 0.8, sr = 0.3 d–1 and ss = 0.005 d–1,
consistent with assignment to Type M. Although specific parameter values for ruthenium
citrate based on in vivo data are available, they are not adopted here, because inhalation
exposure to it is unlikely. Instead, ruthenium citrate is assigned to Type M.
Ruthenium dioxide (RuO2)(30) Bair et al. (1961) followed the biokinetics of 106Ru for 490 days after inhalation of106
RuO2 aerosols by mice. Clearance was initially rapid: ~95% IBB cleared within a few
days. After the first day the lungs contained more 106Ru than any other tissue. Lung retention
was fit by a 3-component exponential function with 83%, 15% and 2% ILD retained withbiological half-times of 7, 28 and 230 days. It was estimated that the ILD was ~25% IBB.
Systemic uptake (bone and muscle) accounted for ~1% IBB at 1 day, and decreased slowly
thereafter. As discussed below, bound state parameter values for ruthenium of fb = 0.05 andsb = 0.1 d–1 are used here. Assuming these values, dissolution parameter values fitted here
were: fr ~0.3, sr ~10 d–1 and ss ~0.001 d–1, consistent with assignment to Type M.
(31) Burykina (1962) measured the tissue distribution of 103Ru at times up 11 days afteradministration of 103RuO2 to rats by intratracheal instillation. There were very low activities
measured in systemic tissues, <0.01% ILD in total, indicating Type S behaviour.
(32) Stuart and Gaven (1970) followed the biokinetics of 106Ru for 39 months after
inhalation of 106RuO2 by dogs. The 106RuO2 was avidly retained in the lungs. After the earlyclearance phases, whole body retention was fit by a single exponential function withbiological half-times in the range 5 - 9 years. From 7 to 39 months >98% of retained 106Ru
was in the lungs or associated lymph nodes. As discussed below, bound state parametervalues for ruthenium of fb = 0.05 and sb = 0.1 d–1 are used here. Assuming these values,
dissolution parameter values fitted here were: fr = 0.0005, sr = 100 d–1 and ss = 0.0004 d–1,
consistent with assignment to Type S.
(33) As outlined above, Newton and Latven (1971) followed the biokinetics of 106Ru for
16 days after inhalation by a dog of 106Ru oxalate aerosols heat-treated at 500°C or 1000°C,
which was thought to convert most of the 106Ru to 106RuO2. In complementary experiments
fractional absorption of 106Ru from the alimentary tract after administration of the samematerials by gavage to dogs were estimated to be ~0.02 and 0.003. Following inhalation,~50% IBB was excreted in the first few days, and the rest with a half-time of ~40 and ~300
days, respectively. At 16 days after inhalation of aerosol formed at 1000°C, 97% of theretained 103Ru was in the lungs, with ~2% in the skeleton and soft tissues combined,
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suggesting either Type M or Type S behaviour. For the particles formed at 500°C, lungretention was somewhat lower and systemic uptake higher.
(34) As outlined above, Newton et al. (1975, 1976) followed the biokinetics of 106Ru for
365 days after inhalation by hamsters of 106Ru oxalate aerosols heat-treated at 600°C or
1100°C. In dissolution tests in vitro (synthetic serum ultrafiltrate at 37°C for 20 days)
dissolution was negligible. At 365 days after inhalation of aerosol formed at 1100°C, ~84%of the retained 106Ru was in the lungs, with ~1% in the skeleton and ~1% in soft tissues. For
the particles formed at 600°C, lung retention was somewhat lower and systemic uptake
higher. As discussed below, bound state parameter values for ruthenium of fb = 0.05 andsb = 0.1 d–1 are used here. Assuming these values, dissolution parameter values fitted here
were: fr = 0.001, sr = 100 d–1 and ss = 0.003 d–1, for the aerosol formed at 1100°C; and fr =0.001, sr = 100 d–1 and ss = 0.0045 d–1, for the aerosol formed at 600°C, consistent withassignment to Type M.
(35) Five workers were monitored for several months following acute inhalation of 106Ru,
thought to be in the form of RuO2 (Hesp and Coote, 1970). In vivo chest counts were started
3–13 days after intake and continued up to 377 days. Measurements of urinary 106Ru werestarted 15–22 days after intake and continued up to 354 days after intake. Long-term retentionof 106RuO2 occurred in the chest, presumably in lungs and lymph nodes. The biological halftime for chest retention averaged 206 days (range 174–428 days). A similar average half-time
was indicated by urinary data. On average, daily loss in urine was equivalent to about 44% ofdaily biological removal from the chest. The other 56% presumably was lost in faeces orretained in systemic tissues. As discussed below, bound state parameter values for ruthenium
of fb = 0.05 and sb = 0.1 d–1 are used here. Assuming these values, dissolution parametervalues fitted here were: fr = 0.001, sr = 100 d–1 and ss = 0.002 d–1, consistent with assignment
to Type M.
(36) As noted in the section on ruthenium tetroxide above, in two reported incidents it
was suspected that RuO4 was released into the environment but converted to RuO2 byinteraction with the ambient aerosol.
(37) Seven persons were monitored by external counting following accidental inhalationof 103Ru (Pusch 1968). Drops of water containing fission products of 235U had been
accidentally spread on a laboratory floor, and 103Ru in the droplets apparently became
airborne and spread throughout the building. The chemical form of airborne 103Ru was notdetermined but may have been a mixture of 103RuO4 vapour and particulate 103Ru, possibly
RuO2 formed by interaction of 103RuO4 with the ambient aerosol through processes describedby Snipes and Kanapilly (1983). Ruthenium was not detected in any organ other than thelungs. Measurements of retention in the chest were started 3 days after exposure andcontinued for 1-4 months. The biological half-time averaged ~80 days (range 64 to 93 days).
Urinary excretion accounted for ~20% of urinary plus faecal losses in the early days after
exposure, suggesting Type M behaviour.
(38) Thirty-five workers were exposed for 10-15 minutes to airborne 106Ru while working
in a building where nuclear fuel was reprocessed (Howells et al., 1977). The released activity
appeared to have been 106RuO4, but this presumably was converted in part to particulate formsof 106Ru during mixing and interacting with room air (Snipes and Kanapilly, 1983). Lateranalysis of samples from the contaminated building indicated that the ruthenium was in anoxide form (Howells et al., 1977). Immediately after the incident, individuals were monitored
by external counting. Localization (longitudinal and lateral scanning) began within 8 days andindicated that the observed 106Ru was retained in the lungs, with no significant translocation
to other body organs. Measurements of chest activities were made on 11 workers for 3 years.
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Biological half-times estimated for seven workers were in the range 625-3500 days. They
were not determined for the other three, because their fitted effective half-times equalled or
exceeded the physical half-life of 106Ru. The apparent increase in lung content was attributed
to redistribution of activity to sites with higher counting efficiency. The long biological halftimes are consistent with the hypothesis that the deposited 106Ru had been converted to106
RuO2, and suggest Type S behaviour.
(39) Based on these studies ruthenium dioxide is assigned to default Type S.
Irradiated fuel fragments(40) Rundo (1965) measured mixed fission products in vivo from 6 to 864 days aftersuspected accidental inhalation of irradiated uranium by a worker. Measurements indicatedthat the activity was mainly located in the lungs. Biological clearance of 103Ru could not bemeasured, suggesting a half-time >230 days, and Type M or S behaviour of the ruthenium
present.
(41) Mirell and Blahd (1989) made whole-body measurements of activity on seven people
from about two weeks to several months after exposure to the initial Chernobyl reactor
accident plume in Kiev, Ukraine. Biological retention half-times were similar for different
radionuclides (45 days for 103Ru) and different from those expected for systemic retention,
indicating that they were trapped in particles and metabolically inert, thus indicating Type M
rather than Type F behaviour.
(42) The in vitro dissolution of samples of particles released from the Chernobyl accident
was measured for up to 60 d (Cuddihy et al., 1989). For all radionuclides, including 103Ru and106
Ru, 10% dissolved in a few hours, and the rest with a half-time of 160 d. Hence fr = 0.1, sr~10 d–1, and ss = 0.004 d–1, consistent with assignment to Type M.
(43) Lang et al, (1994) followed the biokinetics of 95Zr, 95Nb, 103Ru, and 141Ce for 3
months after intratracheal instillation of neutron-irradiated UO2 particles into rats. For the103
Ru the amounts in kidney and bone were <1% ILD. It was assessed here that fr ~0.01, andss ~ 0.005 d–1, suggesting Type M or S behaviour.
(44) Based on these studies ruthenium associated with irradiated fuel fragments is
assigned to default Type M.
Rapid dissolution rate for ruthenium(45) Following deposition in the respiratory tract of the most soluble forms studied(chloride, oxalate and citrate), a rapid phase of dissolution was observed. Analysis heresuggested values of sr of the order of 10-100 d–1, but it was considered that there wasinsufficient information to select a rapid dissolution rate, sr, for ruthenium different from thegeneral default value of 100 d–1, which is applied here to all Type F forms of ruthenium.
Extent of binding of ruthenium to the respiratory tract(46) Following deposition in the respiratory tract of the most soluble forms studied(citrate, chloride and oxalate), a rapid phase of dissolution was observed, but was incomplete.
The strongest evidence that the retention was at least partly due to binding to respiratory tract
tissues, rather than transformation to relatively insoluble particles, comes from studies of
inhaled RuO4. Long-term retention of a fraction of the ruthenium was observed throughout
the respiratory tract, but notably in the ET and conducting airways, from which most particles
are cleared rapidly. Autoradiographs showed that the ruthenium dispersion in the turbinates
and lymph nodes was relatively uniform: only single tracks were observed with no indicationsof focal accumulation, supporting the view that the ruthenium was in a bound rather than18

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particulate form. Based on the results of a study of 106RuO4 inhaled by dogs (Snipes, 1981),
bound state parameter values for ruthenium of fb = 0.05 and sb = 0.1 d–1 were chosen here.
(47) There is experimental evidence that ruthenium in soluble form deposited in the
conducting airways is retained in a bound state. It is therefore assumed here that these boundstate parameter values apply throughout the respiratory tract (ET2, BB, bb and AI regions).
Table 2-2. Deposition and absorption for gas and vapour compounds of ruthenium

Chemical
form/origin
Ruthenium
tetroxide
765
766
767
768
769
770
771
772

Percentage deposited (%)aTotal ET1 ET2 BB bb AI
100b

40

40

12

7

Absorptionb
frsr (d–1)
0.5 1

1

Absorption from thealimentary tract, fA
0.01

aPercentage deposited refers to how much of the material in the inhaled air remains in the body after
exhalation. Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless theydissolve in, or react with, the surface lining.
b
It is assumed that for ruthenium the bound fraction fb is 0.05 with an uptake rate sb = 0.1 d–1.

Table 2-3. Absorption parameter values for inhaled particulate forms of ruthenium and foringested ruthenium

Inhaled particulate materials
Default parameter valuesb,cAbsorption
Assigned forms
TypeF
Chloride, oxalate
M
Citrate, all unspecified formsd
S
DioxideAbsorption
parameter Absorption fromvaluesathealimentaryfrsr (d–1) ss (d–1) tract, fA

1
0.2
0.01

Ingested material
All chemical forms
773
774
775
776
777
778
779
780
781
782
783
784
785
786
787
788
789
790
791

ss (d–1)
0.001

30
3
3

–
0.005
1x10-40.05
0.01
5x10-40.05

a

It is assumed that for ruthenium the bound fraction fb is 0.05 with an uptake rate sb = 0.1 d–1, and that thisapplies throughout the respiratory tract (ET2, BB, bb and AI regions). The values of sr for Type F, M and S
forms of ruthenium (30, 3 and 3 d–1, respectively) are the general default values.
bMaterials (e.g. ruthenium chloride) are listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see text).
c
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of ruthenium (0.05).
dDefault Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

2.2.2. Ingestion(48) Measurements of the urinary and faecal excretion of ruthenium by a male volunteer
after ingestion of chloro-complexes of Ru(III) and Ru(IV), Ru-contaminated clams or nitrosyl
Ru(III) suggested that absorption was about 0.01 and perhaps somewhat greater for nitrosyl
Ru(III) (Yamagata et al, 1969). Studies by Veronese et al. (2003) and Giussani et al. (2008)
used stable isotopes for the determination of the absorption and retention of ruthenium in five19

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
792
793
794
795
796
797
798
799
800
801
802
803
804
805
806
807
808
809
810
811
812
813
814
815
816
817
818
819
820
821
822
823
824
825
826
827
828
829
830
831
832
833
834
835
836
837
838
839

human subjects. They obtained absorption values of (7.5±1.2)·10-3 for inorganic ruthenium(poorly complexed ruthenium), 0.039±0.005 for Ru-citrate, and <0.04 for Ru-ascorbate.
(49) Results from a number of studies of the absorption of 106Ru administered as thechloride to mice, rats, rabbits, guinea pigs, chickens, cats, dogs and monkeys, including
values for fasted animals, were in the range of 0.02 - 0.06 (Burykina, 1962; Thompson et al,
1958; Furchner et al, 1971; Bruce and Carr, 1961; Stara et al, 1971). Values for 106Ru
administered as the oxide to rats and rabbits were in the range of 0.003 - 0.03. Bruce and Carr
(1961), Bruce (1963) measured the absorption of Ru administered in the form of nitrosyl
derivatives. Both nitrato and nitro- complexes of nitrosyl Ru are formed during dissolution in
nitric acid in the reprocessing or U fuels. The nitro-complexes are probably more importantbecause they are more resistant to hydrolysis in neutral and alkaline conditions. Results
obtained for the nitrato-nitrosyl complex in rats and rabbits were 0.06 and 0.13, respectively.
A value of 0.04 was reported for the absorption of Ru administered to rats as a nitro-nitrosyl(Bruce, 1963). Stara et al. (1971) estimated absorption of Ru in cats given nitrosyl Ru
compounds as between 0.1 and 0.15. Cantone et al. (1994) used stable isotopes to estimate
absorption in a rabbit as 0.06.
(50) In Publication 30 (ICRP, 1980), an absorption value of 0.05 was recommended for
all chemical forms of Ru. This value was adopted in Publication 56 (ICRP, 1989) for dietaryintakes. In this report, the default assumption is an fA of 0.05.
2.2.3. Systemic Distribution, Retention and Excretion
2.2.3.1. Summary of the database
Data for human subjects(51) Whole-body retention of ruthenium was measured in a healthy adult male who
ingested different chemical forms of 103Ru (T1/2 = 39.3 d) or 106Ru (T1/2 = 373.6 d) on
different occasions (Yamagata et al., 1969, 1971). Data for 103Ru indicated two retention
components with biological half-times of 2.3 d and 30 d. The early component may havereflected unabsorbed activity, including activity bound in the intestinal mucosa as observed inlaboratory animals after oral administration of ruthenium (Nelson et al., 1962; Bruce et al.,
1962; Stara et al., 1971). The longer-term behavior of 103Ru in the subject could not be
determined due to the short radiological half-life. Results from a later study on the same
subject using 106Ru suggested a retention component with half-time of about 9 d and a second
component with half-life 32 d. At longer times, the estimated biological half-time lengthened
with the period of observation: 81 d based on observations in the period 40-80 d after intake,122 d at 80-150 d after intake, 158 d at 150-350 d after intake, and 385 d at 350-660 d after
intake.
(52) Veronese, Giussani, and coworkers measured the rate of disappearance of the stable
isotope 101Ru from blood plasma and its rate of urinary excretion following intravenous
injection into healthy volunteers (Veronese et al., 2001, 2003, 2004; Giussani et al., 2008).
Solutions with different degrees of complexation of ruthenium with citrate were injected indifferent experiments. In all cases there was an initial rapid distribution of ruthenium
between plasma and the interstitial fluids. The subsequent pattern of disappearance fromplasma depended on the form administered. A relatively fast component of clearance wasfollowed by a relatively slow phase, but the ratio of the size of the fast and slow components
varied with the degree of complexation of ruthenium in the injected solution. The
investigators concluded that the fast and slow components represented ruthenium complexed
20

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
840
841
842
843
844
845
846
847
848
849
850
851
852
853
854
855
856
857
858
859
860
861
862
863
864
865
866
867
868
869
870
871
872
873
874
875
876
877
878
879
880
881
882
883
884
885
886
887

with citrate and inorganic ruthenium, respectively. The half-times of the fast and slow
components of clearance were estimated as 17 +/- 2 min (mean +/- standard deviation) and 23+/- 2 h, respectively. The fast component represented an estimated 82 +/- 2% of the total forsolutions with highly complexed ruthenium and 17 +/- 2% for solutions with the lowest
degree of complexation. Urinary excretion of ruthenium was rapid following injection ofhighly complexed ruthenium, with more than 40% of the injected amount excreted in urine
during the first 12 h and up to 70% over the first 2 d. Total excretion amounted to less than
25% of the injected amount over the first 48 h after administration of the solution with thelowest degree of complexation.
Data for laboratory animals(53) Furchner et al. (1964, 1971) investigated the systemic biokinetics of 106Ru in mice,
rats, monkeys, and dogs receiving 106RuCl3 orally or by intraperitoneal or intravenous
injection. For each species, whole-body retention data from injection studies were fit by asum of four exponential terms. Short- and intermediate-term retention as represented by the
first three terms was broadly similar in the four species. Long-term retention represented
about 17% (14.7-18.7%) of the injected amount in all four species, but corresponding
biological half-times were more variable: about 750 d in mice, 500 d in rats, 200 d inmonkeys, and 1500 days in dogs. The large differences in derived long-term half-times may
have been due in part to the different lengths of observation periods, e.g. 276 d for monkeys
and 970 d for dogs, but this does not fully explain the differences.
(54) Boecker and Harris (1969) investigated the behavior of 106Ru in beagles after acuteinhalation of 106Ru citrate. By a few days after intake the systemic burden represented the
preponderance of total-body activity although the concentration of 106Ru in the lungs
exceeded that in other tissues throughout the 512-day study. A sum of four exponential terms
fit to whole-body retention data paralleled a retention curve determined earlier by Furchner etal. (1964) for dogs receiving 106RuCl3 by intravenous injection. As determined in one of thedogs in the inhalation study, losses by urinary and faecal excretion were roughly the sameover the first three days, but thereafter daily urinary excretion generally was 3-7 times greaterthan daily faecal excretion.
(55) Cumulative urinary excretion over the first 3 d after intravenous or intraperitoneal
injection of 106RuCl3 into monkeys, dogs, rats, and mice was 21.6-29.0% of the injectedamount (Furchner et al., 1971). Cumulative faecal excretion was more variable, ranging from
4.1% in dogs to 18.7% in mice. The urinary to faecal excretion ratio over the first three days
was 2.6 in monkeys, 5.5 in dogs, 2.2 in rats, and 1.6 in mice.
(56) In guinea pigs receiving 106RuCl3 by subcutaneous injection, about two-thirds of theinjected ruthenium was excreted in urine and faeces over the first 47 d (Burykina, 1962). The
urinary to faecal excretion ratio during that period was 2.7.
(57) In rats, cumulative urinary excretion over the first 60 d accounted for 53.8% of theadministered amount after intravenous injection and 51.8% after intraperitoneal injection of106
Ru as chlorides (Thompson et al., 1958). The urinary to faecal excretion ratio during thesame period was 2.8 for intravenous injection and 2.4 for intraperitoneal injection.
(58) Compared with intravenous or intraperitoneal injection data for ruthenium chlorides,
higher rates of urinary and faecal excretion have been estimated for activity absorbed to blood
after inhalation of 106Ru as ruthenium tetroxide vapor (RuO4) by rats (Runkle et al. (1980) or
dogs (Snipes, 1981). The systemic distribution of retained 106Ru was broadly similar to that
determined in injection studies involving other forms of ruthenium.
(59) The time-dependent distribution of ruthenium in systemic tissues and fluids has been
21

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
888
889
890
891
892
893
894
895
896
897
898
899
900
901
902
903
904
905
906
907
908
909
910
911
912
913
914
915
916
917
918
919
920
921
922
923
924
925
926
927
928
929
930
931
932
933
934
935

studied in several animal species including mice, rats, rabbits, hamsters, guinea pigs, anddogs (Durbin et al., 1957; Thompson et al., 1958; Durbin, 1960; Bair et al., 1961; Bruce andCarr, 1961; Nelson et al., 1962; Burykina, 1962; Bruce, 1963; Seidel et al., 1963; Boecker
and Harris, 1969; Furchner et al., 1971; Newton et al., 1976; Runkle and Snipes, 1978;
Runkle et al., 1980; Snipes, 1981). A relatively high concentration of ruthenium in blood isindicated in some studies (Burykina, 1962; Newton and Latven, 1971; Snipes, 1981). Liverand kidneys are important repositories for ruthenium in the early days and weeks following its
absorption to blood. Bone has been identified as an important long-term repository forruthenium in some studies (Thompson et al., 1958; Bair et al., 1961; Burykina, 1962; Boecker
and Harris, 1969). Reported fractions of systemic activity in liver, kidneys, and bone at any
given time after intake are variable. For example, the liver contained roughly 6% of theadministered activity at 2 d after intraperitoneal injection of 106Ru as chloride into rats
(Furchner et al., 1971) but about 19-26% of the absorbed activity at 1-3 days after
subcutaneous injection of 106Ru as chloride into guinea pigs (Burykina, 1962). Muscle andskin generally show much lower concentrations than liver and kidneys, particularly at earlytimes after uptake to blood, but usually contain much or most of the systemic activity due totheir large mass (Burykina, 1962; Boecker and Harris, 1969; Furchner et al., 1971). Nelson etal. (1962) concluded from an autoradiographic study of mice given 103Ru chloride byintravenous injection that the distribution pattern of ruthenium is determined to a large extent
by its elevated uptake and retention in connective tissues.
(60) Thompson et al. (1958) concluded from studies of rats administered 106Ru chlorides
by different modes that activity was retained more tenaciously in bone tissue than in visceralorgans of rats and that deposition was greater in bone of young growing rats than in older
animals. After oral administration of ruthenium as nitrosyl-trinitrate to rabbits, theconcentration of ruthenium in bone was not uniform but highest in the ends of bones,
apparently associated with higher deposition in areas of better blood supply and possibly bone
growth (Bruce and Carr, 1961). Nelson et al. (1962) found in an autoradiographic study on
mice given 103Ru chloride by intravenous injection that the concentration of 103Ru was low in
cortical bone but that the epiphyseal plates had significant early uptake and the periosteal
layer had marked activity throughout the 32-day period of observation. In relatively longterm studies, activity in bone usually has represented a substantial portion of the systemic
content of ruthenium at times remote from intake (Thompson et al., 1958; Bair et al., 1961;
Burykina, 1962; Boecker and Harris, 1969), but there are exceptions. For example, in a study
on rats, activity in bone was estimated to represent at most 8.4% of systemic activity during
the first 283 d after intraperitoneal injection of 106Ru as chloride (Furchner et al., 1971). By
contrast, in guinea pigs receiving 106Ru as chloride by subcutaneous injection, activity in bone
was estimated to represent about 40% of the systemic activity at 50 d after administration. At
128-512 d after inhalation of 106Ru as citrate by dogs, activity in the skeleton represented
nearly 30% of the systemic activity as estimated from data for muscle, pelt, liver, kidneys,and gastrointestinal tract.
2.2.3.2. Biokinetic model for systemic ruthenium(61) The biokinetic model for systemic ruthenium is taken from a paper by Leggett(2012). The model structure is shown in Figure 2-1. Transfer coefficients are listed in Table
2-4.
(62) The model for blood is based on data of Veronese et al. (2003, 2004) on the rate ofdisappearance of ruthenium from blood plasma following intravenous injection of different
22

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
936
937
938
939
940
941
942

943
944
945
946

forms of ruthenium. Model parameter values are based on data for the form removed mostslowly from plasma (a solution with a low degree of complexation of ruthenium with citrate),in view of the prolonged retention of ruthenium in blood indicated by some inhalation or
injection studies on laboratory animals (Burykina, 1962; Newton and Latven, 1971; Snipes,
1981). Retention components determined for blood plasma in the human study are assumed toapply to whole blood.

Figure 2-1. Structure of the biokinetic model for systemic ruthenium.

23

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
947

Table 2-4. Transfer coefficients for systemic ruthenium
From
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 2
Liver 0Liver 0Liver 0Liver 1
Urinary path
Other kidney tissue
ST0
ST1
ST2
Cortical bone surface
Trabecular bone surface
Cortical bone surface
Trabecular bone surface
Cortical bone volume
Trabecular bone volume
948
949
950
951
952
953
954
955
956
957
958
959
960
961
962
963
964
965
966

To
Small intestine contents
Urinary bladder contents
Liver 0Kidney urinary path
Other kidney tissue
Blood 2
ST0
ST1
ST2
Cortical bone surface
Trabecular bone surface
Blood 1
Blood 1
Small intestine contents
Liver 1
Blood 1
Urinary bladder contents
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Cortical bone volume
Trabecular bone volume
Blood 1
Blood 1

Transfer coefficient (d-1)
3.0
17
12
7.76
0.24
27
15
5.0
5.0
2
6
0.6931
0.09704
0.03466
0.006931
0.003798
0.13860.003798
0.099020.02310.0009495
0.079220.079220.01980.01980.0000821
0.000493(63) In the model, blood is divided into two compartments called Blood 1 and Blood 2.
Ruthenium entering blood is assigned to Blood 1, which is a rapid-turnover pool. Blood 2 isa more slowly exchanging pool that contains most of the activity in blood except for a shortperiod soon after acute uptake of ruthenium. Activity leaves Blood 1 at the rate 100 d-1,
corresponding to a half-time of ~10 min, with 27% of outflow going to Blood 2 and theremaining 73% divided among tissue compartments, urinary bladder contents, andgastrointestinal contents. Activity moves from Blood 2 back to Blood 1 with a half-time of 1d.
(64) Urinary excretion is assumed to arise from transfer of activity from blood into theurinary bladder contents and transfer from blood to the kidneys (Urinary path) and subsequent
release to the urinary bladder contents over a period of days. Faecal excretion is assumed toarise in part from biliary secretion of ruthenium into the small intestine contents after uptake
by the liver and in part from secretion from Blood 1 into the small intestine contents.
Parameter values for urinary and faecal excretion are set so that: model predictions are in
reasonable agreement with early urinary data for a human subject injected with lowcomplexed Ru and for monkeys, dogs, rats, and mice injected with 106Ru; urinary excretion
represents about 80% of total excretion based on data for different animal species but withdata for dogs and monkeys given relatively high weight; and the two sources of faecal

24

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
967
968
969
970
971
972
973
974
975
976
977
978
979
980
981
982
983
984
985
986
987
988
989
990
991
992
993
994
995
996
997
998
999
1000
1001
1002
1003
1004
1005
1006
1007
1008
1009
1010
1011
1012
1013
1014

excretion contribute equally to endogenous faecal excretion of ruthenium, in the absence ofspecific data on relative contributions of these sources.
(65) The distribution of ruthenium leaving blood is based to a large extent on the timedependent distribution of ruthenium determined in laboratory animals, particularly dogs
because of the availability of relatively long-term data for dogs. In addition to the 27% ofoutflow from Blood 1 assigned to Blood 2, outflow from Blood 1 is distributed as follows:
12% to Liver, 8% to Kidneys, 8% to Bone, 17% to the Urinary bladder contents, 3% to Small
intestine contents, and 25% to Other. Activity entering Liver is assigned to the rapid-turnover
liver compartment called Liver 0. Fractions 0.97 and 0.03 of activity entering Kidneys are
assigned to Urinary path and Other kidney tissue, respectively. Three-fourths of activity
entering bone is assigned to Trabecular bone surface and one-fourth to Cortical bone surface.
Activity entering Other (25% of outflow from Blood 1) is divided as follows: 15% to theshort-term retention compartment ST0; 5% to the intermediate-term compartment ST1, and
5% to the long-term retention compartment ST2.
(66) Biological half-times for compartments are set to reproduce different phases of lossof ruthenium from the total body observed in laboratory animals and a human subject, and thetime-dependent distribution of systemic activity in dogs. Activity is removed from Liver 0
with a biological half-time of 5 d, with 25% going to the Small intestine contents (biliary
secretion), 5% to Liver 1, and 70% to Blood 1. Activity transfers from Liver 1 to Blood 1
with a half-time of 0.5 y. Activity transfers from Urinary path to Urinary bladder contents
with a half-time of 5 d and from Other kidney tissues to Blood 1 with a half-time of 0.5 y.
Activity in soft-tissue compartments ST0, ST1, and ST2 returns to Blood 1 with half-times of
7 d, 30 d, and 2 y, respectively. Activity leaves Cortical bone surface or Trabecular bone
surface with a half-time of 7 d, with 80% transferring to Blood 1 and 20% to thecorresponding bone volume compartment. Activity transfers from Cortical bone volume or
Trabecular bone volume to Blood 1 at the rate of bone turnover.
2.2.3.3. Treatment of radioactive progeny(67) The radioactive progeny addressed in the derivation of dose coefficients forruthenium isotopes are all isotopes of rhodium or technetium. Rhodium and ruthenium have
similar chemical properties and appear from limited comparative data to have broadly similar
biokinetics in rats. Therefore, rhodium produced in systemic compartments by decay ofruthenium is assigned the biokinetic model for ruthenium. Technetium atoms produced in asystemic compartment of the ruthenium model that is identifiable with a compartment of thecharacteristic model for technetium (i.e. the model applied in this report to technetium as aparent radionuclide) are assigned the characteristic model for technetium from their time of
production. Technetium atoms produced in compartments of the ruthenium model that are
ambiguous with regard to the characteristic model for technetium are assigned a transfer
coefficient to the blood compartment of the technetium model, named Blood, and uponreaching Blood are assigned the characteristic model for technetium. For modelingconvenience, the blood compartment of the technetium model is identified with the central
blood compartment of the ruthenium model, named Blood 1. Technetium atoms produced incompartments of the liver, kidneys, or other soft tissues of the ruthenium model are assumed
to transfer to Blood with a half-time of 1.6 d, the shortest removal half-time from other soft
tissue in the technetium model. Technetium atoms produced in Blood 2 of the ruthenium
model are assumed to transfer to Blood at the rate 1000 d-1, a default value used in this report
to represent rapid biological removal.
25

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1015
1016
1017
1018
1019
1020
1021
1022

2.3. Individual monitoring
106

Ru(68) 106Ru is a beta emitter but it is by measured using the 0.512 and 0.622 MeV gamma
rays from its short-lived daughter, 106Rh. Urine bioassay and/or Whole Body counting may be
used to estimate the content of 106Ru internally deposited in the body.
Isotope
106

Ru

106

Ru

106

Ru

1023
1024
1025
1026
1027
1028
1029
1030
1031
1032
1033
1034
1035
1036
1037
1038
1039
1040
1041
1042
1043
1044
1045
1046
1047
1048
1049
1050
1051
1052
1053
1054
1055
1056

Monitoring
Technique

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
γ-ray spectrometry 10 Bq/L
of 106Rh
Whole
Body γ-ray spectrometry 200 Bq
Countingof 106Rh
Lung Counting
γ-ray spectrometry 42 Bq*
of 106Rh

Achievabledetection limit
3 Bq/L
130 Bq∗ Lung monitoring of 106Ru is not generally used in routine monitoring of workers. Monte Carlo program
Visual Monte Carlo was used to simulate the photon emission, to calculate the calibration factor for thegeometry and radionuclide, and to calculate the minimum detectable activity (MDA) in the lung. (Hunt et al,2012)

References
Bair, W.J., Willard, D.H., Temple, L.A., 1961. The behavior of inhaled 106RuO2 particles. HealthPhys. 5:90-98.
Boecker, B.B., Harris, A.M., 1969. Tissue distribution, excretion and dosimetry of inhaled 106Ru
citrate in the beagle dog. In: Fission Product Inhalation Program Annual Report, 1968-1969.
LF-41. pp. 111-116. Lovelace Foundation for Medical Education and Research, Albuquerque,
New Mexico. Available from National Technical Information Service, Springfield, Virginia.
Bruce, R.S., 1963. Some factors influencing the absorption, retention and elimination of ruthenium.
In: Diagnosis and treatment of radioactive poisoning. Vienna:IAEA, pp. 207-244.
Bruce, R.S., Carr, T.E.F., 1961. Studies in the metabolism of carrier-free radioruthenium - II. The
uptake of nitrosyl-ruthenium complexes from the gastrointestinal tract. Reactor Science andTechnology 14, 145-154.
Bruce, R.S., Carr, T.E.F., Collins, M.E., 1962. Studies in the metabolism of carrier-freeradioruthenium - III. The behavior of nitrosyl-ruthenium in the gastrointestinal tract. HealthPhys. 8, 397-406.
Burykina, L.N., 1969. On the problem of the toxicity of ruthenium-106 under repeated intratracheal
administration to rats. In: Radioactive isotopes and the body, Moskalev, Yu. I., ed. Izdatel’stvo
Medisina, Moscow. AEC-tr-7195, United States Atomic Energy Commission Division ofTechnical Information, pp. 388-396.
Burykina, L.N., 1962. The metabolism of radioactive ruthenium in the organism of experimental
animals. In: The Toxicology of Radioactive Substances, Vol. 1 (A.A. Letavel and E.P.
Kurlyandsicaya, Eds.) pp 60-76. Pergamon Press, Oxford.
Cantone, M.C., de Bartolo, D., Gambarini, G., Giussani, A., Ottolenghi, A., Pirola, L., Hansen, Ch.,
Roth, P., Werner, E., 1994. Proton nuclear activation in stable tracer technique for ruthenium
metabolism studies. Nucl. Instrum. Methods Phys. Res., Sect. A. 353 (1-3), 440-443.
Cuddihy, R.G., Finch, G.L., Newton, G.J., Hahn, F.F., Mewhinney, J.A., Rothenberg, S.J., Powers,
D.A., 1989. Characteristics of radioactive particles released from the Chernobyl nuclear
reactor. Environ. Sci. Technol. 23 (1), 89-95.

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1057
1058
1059
1060
1061
1062
1063
1064
1065
1066
1067
1068
1069
1070
1071
1072
1073
1074
1075
1076
1077
1078
1079
1080
1081
1082
1083
1084
1085
1086
1087
1088
1089
1090
1091
1092
1093
1094
1095
1096
1097
1098
1099
1100
1101
1102
1103
1104
1105
1106
1107
1108

Dobryakova, G.V., 1970. Dynamics of the removal of Te-127 and Ru-106 from rat lungs. In:
Moskalev, Yu. I., Editor. Radioaktiv. Izotopy Vnesh. Srede Organizme. pp. 57-63. Moscow:
Atomizdat.
Durbin, P.W., 1960. Metabolic characteristics within a chemical family. Health Phys. 2:225-238.
Durbin, P.W., Scott, K.G., Hamilton, J.G., 1957. Distribution of radioisotopes of some heavy metals
in the rat. University of California (Berkely) Publ. Pharmocol. 3, 1-34.
Furchner, J.E., Richmond, C.R., Drake, G.A., 1964. Ruthenium-106 in mice, rats, and dogs:
Interspecies comparisons. LA-3132-MS, Los Alamos Scientific Laboratory, Los Alamos, NM,
pp. 19-24.
Furchner, J.E., Richmond, C.R., Drake, G.A., 1971. Comparative metabolism of radionuclides inmammal-VII. Retention of 106-Ru in the mouse, rat, monkey and dog. Health Phys. 21, 355365.
Giussani, A., Cantone, M.C., Gerstmann, U., Greiter, M., Hertenberger, R., Höllriegl, V., Leopold,
K., Veronese, I., Oeh, U., 2008. Biokinetics of ruthenium isotopes in humans and its
dependence on chemical speciation. 12th International Congress of the International Radiation
Protection Association, IRPA 12, Buenos Aires, Argentina, 19-24 October 2008 (Proceedings
on CD).
Hesp, R., Coote, J., 1970. Body radioactivity studies on a series of cases in which ruthenium-106
oxide was inhaled.
Health Safety Dep., U. K. At. Energy Auth.,Sellafield/Seascale/Cumberland, Engl. U. K. At. Energy Auth., Prod. Group, PG Rep. No. 979
W.
Howells, H., Ward, F.A., Coulston, D.J., Woodhouse, J.A., 1977. In-vivo measurement and dosimetryof ruthenium-106 oxide in the lung. In: Proceedings of a symposium on the handling ofradiation accidents. Vienna: International Atomic Energy Agency. IAEA-SM-215/54, pp. 83102.
ICRP, 1980. International Commission on Radiological Protection. Limits on Intakes ofRadionuclides for Workers. ICRP Publication 30, Pt.2. Pergamon Press, Oxford. Ann. ICRP 4,(3/4).
ICRP, 1989. International Commission on Radiological Protection. Age-dependent Doses toMembers of the Public from Intake of Radionuclides. Pt.1. ICRP Publication 56. Pergamon
Press, Oxford. Ann. ICRP 20, (2).
ICRP, 2002. Guide for the Practical Application of the ICRP Human Respiratory Tract Model. ICRP
Supporting Guidance 3 Ann. ICRP, 32(1-2).
Lang, S., Kosma, V.M., Kumlin, T., Halinen, A., Salonen, R.O., Servomaa, K., Rytomaa, T.,
Ruuskanen, J., 1994. Distribution and short-term effects of intratracheally instilled neutronirradiated UO2 particles in the rat. Environ. Res. 65 (1), 119-31.
Mirell, S.G., Blahd, W.H., 1989. Biological retention of fission products from the Chernobyl plume.
Health Phys. 57 (4), 649-52.
Nelson, A., Ullberg, S., Kristoffersson, H., Ronnback, C., 1962. Distribution of radioruthenium in
mice. Acta Radiol. 58, 53-360.
Newton, G.J., Latven, R.K., 1971. Distribution and excretion in the beagle dog of 106Ru-Rh aerosols
subjected to thermal degradation. In: Fission Product Inhalation Program Annual Report, 19701971. LF-144. Albuquerque, NM: Lovelace Foundation, pp. 81-85.
Newton, G.J., Servilla, P., Wagner, J., Boecker, B.B., 1975. Radiation dose patterns from 106Ru
aerosols inhaled by Syrian hamsters. I. In: Inhalation Toxicology Research Institute Annual
Report 1974-1975. LF-52. Albuquerque, NM: Lovelace Biomedical and Environmental
Research Institute, pp. 75-78.
Newton, G.J., Snipes, M.B., Boecker, B.B., Wagner, J.A., 1976. Radiation dose patterns from 106Ru
aerosols inhaled by Syrian hamsters. II. Retention and distribution. In: Inhalation Toxicology
Research Institute Annual Report 1975-1976. LF-56. Albuquerque, NM: Lovelace Biomedical
and Environmental Research Institute, pp. 79-83.
Pollanen, R., 1997. Highly radioactive ruthenium particles released from the Chernobyl accident:

27

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1109
1110
1111
1112
1113
1114
1115
1116
1117
1118
1119
1120
1121
1122
1123
1124
1125
1126
1127
1128
1129
1130
1131
1132
1133
1134
1135
1136
1137
1138
1139
1140
1141
1142
1143
1144
1145
1146
1147
1148
1149
1150
1151
1152

particle characteristics and radiological hazard. Radiat. Prot. Dosim. 71(1), 23-32
Pusch, W.M., 1968. Determination of effective half-life of ruthenium-103 in man after inhalation.
Health Phys. 15 (6), 515-17.
Rundo, J., 1965. A case of accidental inhalation of irradiated uranium. Brit. J. Radiol. 38, 39–50.
Runkle, G.E., Snipes, M.B., 1978. Dose patterns for 106RuO4 inhaled by Fischer-344 rats and beagle
dogs. In: Inhalation Toxicology Research Institute Annual Report. LF-60. Albuquerque, NM:
Lovelace Biomedical and Environmental Research Institute, pp. 55-60.
Runkle, G.E., Snipes, M.B., McClellan, R.O., Cuddihy, R.G., 1980. Metabolism and dosimetry of
inhaled 106RuO4 in Fischer-344 rats. Health Phys. 39, 543-553.
Seidel, D., Catsch, A., Schweer, K.H., 1963. [Decorporation of radionuclides (studies onradioruthenium)] Strahlentherapie 122, 595-610.
Snipes, M.B., 1981. Metabolism and dosimetry of ruthenium-106 inhaled as ruthenium-106
tetraoxide by beagle dogs. Health Phys. 41 (2), 303-317.
Snipes, M.B., Kanapilly, G.M., 1983. Retention and dosimetry of ruthenium-106 inhaled along withinert particles by Fischer-344 rats. Health Phys. 44 (4), 335-348.
Snipes, M.B. Runkle, G.E., Sproul, S.M., 1977. Deposition, retention and dosimetry of inhaledruthenium aerosols. In: Inhalation Toxicology Research Institute Annual Report, 1976-1977.
LF-58, UC-48. Albuquerque, NM: Lovelace Biomedical and Environmental Research Institute,pp. 22-26.
Stara, J.F., Nelson, N.S., Krieger, H.L., Kahn, B., 1971. Gastrointestinal absorption and tissue
retention of radioruthenium. In: Skoryna, S. C., Waldron-Edward, D. Intestinal absorption of
metal ions, trace elements and radionuclides. Oxford and New York: Pergamon Press, pp. 307318.
Stuart, B.O., Gavin J.C., 1970. Long-term retention and translocation of inhaled 106Ru-106RhO2 inbeagles. Pacific Northwest Lab. Report, BNWL-1050, 3.43-3.45.
Thompson, R.C., Weeks, M.H., Hollis, L., Ballou, J.F., Oakley, W.D., 1958. Metabolism ofradioruthenium in the rat. Am. J. Roentgen. 79, 1026-1044.
Veronese, I., Cantone, M.C., Giussani, A., Maggioni, T., Birattari, C., Bonardi, M., Groppi, F.,
Garlaschelli, L., Werner, E., Roth, P., Höllriegl, V., Louvat, P., Felgenhauer, N., Zilker, Th.,
2003. Stable tracer investigations in humans for assessing the biokinetics of ruthenium andzirconium radionuclides. Rad. Prot. Dosim. 105, 209–212.
Veronese, I., Giussani, A., Cantone, M.C., Birattari C., Bonardi M., Groppi, F., Höllriegl V., Roth, P.,
Werner, E., 2004. Influence of the chemical form on the plasma clearance of ruthenium inhumans. App. Radiat. Isot. 60, 7-13.
Veronese, I., Giussani, A., Cantone, M.C., De Bartolo, D., Roth, P., Werner, E., 2001. Kinetics ofsystemic ruthenium in human blood using a stable tracer. J. Radiol. Prot. 21:31-38.
Webber, C. E., Harvey, J.W., 1976. Accidental human inhalation of ruthenium tetroxide. HealthPhys. 30, 352-355.
Yamagata, N., Iwashima, K., Iinuma, T.N., Watari, K., Nagai, T., 1969. Uptake and retention
experiments of radioruthenium in man -I. Health Phys. 16, 159-166.
Yamagata, N., Iwashima, K., Iinuma, T. A., Ishihara, T., Watari, K., 1971. Long-term retention ofradioruthenium in man. Health Phys. 21:63.

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1153

3.

1154
1155
1156
1157
1158
1159
1160
1161
1162
1163
1164
1165
1166
1167

3.1. Chemical Forms in the Workplace(69) Antimony is a semi-metal or metalloid which mainly occurs in oxidation states III,IV and V. Antimony may be encountered in industry in a variety of chemical and physicalforms, such as oxides, sulphides, chlorides, fluorides, tartrate and trihydride. It may also be
encountered in two anionic forms which are (SbO2-) and (SbO3-). 124Sb and 125Sb are fission
products which may be associated with irradiated fuel or corrosion products. 125Sb also occurs
as a neutron activation product of tin which may be present in reactor components containing
zirconium.
Table 3-1. Isotopes of antimony addressed in this report
Isotope
Sb-115
Sb-116
Sb-116m
Sb-117
Sb-118m
Sb-119
Sb-120
Sb-120m
Sb-122
Sb-124aSb-124n
Sb-125aSb-126
Sb-126m
Sb-127
Sb-128
Sb-128m
Sb-129
Sb-130
Sb-131

1168
1169
1170
1171
1172
1173
1174
1175
1176
1177
1178
1179
1180
1181

Antimony (Z = 51)aPhysical half-life
32.1 m15.8 m60.3 m2.80 h5.00 h38.19 h15.89 m5.76 d2.724 d60.20 d20.2 m2.759 y12.35 d19.15 m3.85 d
9.01 h10.4 m4.40 h39.5 m
23.03 mDecay mode
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+EC
EC, B+EC
B-, EC, B+
BIT
BBB-, IT
BBB-, ITBBB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

3.2. Routes of Intake
3.2.1. Inhalation
Absorption Types and parameter values(70) Information is available from experimental studies of antimony inhaled by laboratory
animals as chloride, tartrate or oxide. Studies of workers occupationally exposed to stable
antimony have been summarised by IARC (1989). Some information is also available on the
behaviour of inhaled 125Sb in man.
(71) Absorption parameter values and Types, and associated fA values for particulate
29

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1182
1183
1184
1185
1186
1187
1188
1189
1190
1191
1192
1193
1194
1195
1196
1197
1198
1199
1200
1201
1202
1203
1204
1205
1206
1207
1208
1209
1210
1211
1212
1213
1214
1215
1216
1217
1218
1219
1220
1221
1222
1223
1224
1225
1226
1227
1228
1229

forms of antimony are given in Table 3-2.
Antimony chloride(72) Djurić et al. (1962) followed the biokinetics of 124Sb after inhalation by rats of
antimony chloride for 140 days. From the results, absorption parameter values calculated by
the task group were fr ~ 1, and sr ~ 0.5 d–1. About 1% of the initial lung deposit (ILD) was
retained in the lungs with a half-time of about 70 days, giving assignment to Type F.
However, from about 2 weeks after intake the concentration of 124Sb in the blood was higher
than that in the lungs, and hence the long-term lung retention observed may have been largely
due to 124Sb in the blood.
Antimony tartrate(73) Felicetti et al. (1974b) followed the biokinetics of 124Sb after inhalation by hamstersof trivalent and pentavalent antimony tartrate aerosols (heat-treated at 100°C) for 32 days. In
complementary experiments with the same materials, absorption in the GI tract was found to
be only about 1%. In contrast, both forms showed similar, rapid absorption from the lungs:
the authors noted that by 2 hours post exposure less than 1% of the initial body burden (IBB)
remained in the lungs, indicating fr ~1, and sr >10 d–1. It was also noted that there wasconsiderable faecal excretion and hence limited absorption in the upper respiratory tract,indicating sr <100 d–1. A central value for sr of 30 d–1 is adopted here. It was estimated herethat about 1% of the of the ILD was retained in the lungs at 2 days and 0.1% ILD at 32 days,
and calculated that fr ~0.99, and ss ~0.1 d–1, giving assignment to Type F. Although similarlung clearance was observed for the two forms, some differences in the systemic tissue
distribution, e.g. between liver and skeleton, were noted.
(74) Thomas et al. (1973) and Felicetti et al. (1974a) followed the biokinetics of 124Sb
after inhalation, by mice and dogs respectively, of aerosols formed by heat-treating antimony
tartrate droplets at various temperatures. For each aerosol, groups of mice were killed atintervals to 52 d, and one dog was killed at 32, 64 and 128 d. The chemical form of theantimony after heat treatment was not determined, but the aerosol treated at the lowest
temperature (100°C) was referred to as tartrate. From the results in mice, it was estimatedhere that about 1% ILD was retained in the lungs at 2 days and 0.03% ILD at 32 days, andcalculated that that fr ~0.99, and ss ~0.1 d–1 (as for the hamster study above). Insufficient
information was given to estimate absorption parameter values in dogs, but at 32 d, 0.23%
ILD was retained, giving assignment to Type F.
(75) Although specific parameter values for antimony tartrate based on in vivo data are
available, they are not adopted here, because inhalation exposure to it is unlikely. Instead,antimony tartrate is assigned to Type F.
Antimony oxides(76) Newton et al. (1994) measured the accumulation and retention of stable antimony
trioxide (Sb2O3) in the lungs of rats during 13 weeks inhalation exposure and for 28 weeks
after exposure. It was estimated here, from measurements in the group exposed to the lowest
concentration (0.25 mg m–3), that the lung retention half-time was about 50 d, indicating TypeM or S behaviour.
(77) Groth et al. (1986) measured the accumulation of antimony in the lungs of rats after
9 months of chronic inhalation exposure to stable Sb2O3. Concentrations in lungs wereconsiderable higher than in any other tissue. It was estimated here that the lung retention halftime was about 50 d, indicating Type M or S behaviour.
30

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1230
1231
1232
1233
1234
1235
1236
1237
1238
1239
1240
1241
1242
1243
1244
1245
1246
1247
1248
1249
1250
1251
1252
1253
1254
1255
1256
1257
1258
1259
1260
1261
1262
1263
1264
1265
1266
1267
1268
1269
1270
1271
1272
1273
1274
1275
1276
1277

(78) Rose and Jacobs (1969) followed whole-body retention of 124Sb for 300 d in one
worker exposed to an aerosol, said to be oxide, resulting from activation of antimony
contamination on a 60Co source. The authors assessed that during the period 10 d to 6 weeks,
there was significant absorption and excretion in urine, but that subsequently the nontransportable activity was retained in the lungs where it decreased only with the physical halflife. This indicates that the overall behaviour might be Type M or S, but there is insufficient
information to determine which.
(79) Smelter workers exposed by inhalation to stable antimony trioxide and pentoxide
showed a positive relationship between measured antimony lung content and period of
employment such that there was about a tenfold increase for 40 y of employment (McCallum
et al., 1971). This indicates that at least some of the material was retained in the lungs on atime-scale of years. Other workers with pulmonary changes related to exposure to antimony
trioxide had measured urinary excretion of antimony in hundreds of μg/l both during and after
employment (McCallum, 1963). This indicates that there is also significant absorption of
antimony from the material in the lungs. Although the human data suggest possible Type M
and S behaviour, the paucity of results do not provide a basis for firmer classification.
Antimony sulphide(80) Groth et al. (1986) measured the accumulation of antimony in the lungs of rats after
9 months of chronic inhalation exposure to stable antimony ore concentrate, which isprincipally antimony trisulphide (stibnite) Sb2S3. Concentrations in lungs were considerable
higher than in any other tissue. It was estimated here that the lung retention half-time wasabout 20 d, indicating Type M behaviour. Compared to rats exposed to oxide in a similar
study (see above), the lung concentrations were lower, but concentrations in other tissues
were similar, suggesting that the sulphide dissolved faster in the lungs than the oxide.
Other compounds(81) As noted above, Thomas et al. (1973) and Felicetti et al. (1974a) followed the
biokinetics of 124Sb following inhalation, by mice and dogs respectively, of aerosols formedby heat-treating droplets of antimony tartrate aerosols at various temperatures. The chemical
form of the antimony after heat treatment was not determined, but the higher temperatures,
500°C and ~1,000°C, were expected to result in an oxide form (Felicetti et al, 1974a). From
the results in mice, it was estimated here that for aerosols formed at both the higher
temperatures (500°C and 1,100°C) ~5% ILD was retained in the lungs at 2 days and ~1% ILD
at 32 days, and it was calculated that fr ~0.95, sr ~3 d–1, and ss ~0.03 d–1. Absorption was thus
considerably slower than for the tartrate aerosols formed at 100°C, but still gave assignment
to Type F. Insufficient information was given to estimate absorption parameter values indogs, but at 32 d after inhalation of the aerosols formed at the higher temperatures (500°C and1,000°C), 25% and 5% ILD was retained in the lungs, giving assignment to Types M and F
respectively.
(82) Garg et al. (2003) followed whole-body retention of 125Sb for 200–2400 d in sevenworkers exposed to an aerosol (probably oxide) produced by saw-cutting of an irradiatedzirconium alloy pressure tube. Detailed measurements indicated that most of the retained
activity was in the lungs, even at a year after intake. The authors assessed that lung retention
at 180 days after intake was 58-91% of the initial alveolar deposit (estimated from the lungcontent at 7 d after intake), giving assignment to Type S in each person. However, as the125
Sb and parent tin were presumably minor constituents of the zirconium alloy, the particle
matrix might well have been predominantly oxides of other metals (and/or the metals
31

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1278
1279
1280
1281
1282
1283
1284
1285
1286
1287
1288
1289
1290
1291
1292

themselves), notably zirconium, which has a highly insoluble oxide (see zirconium section).
Rapid dissolution rate for antimony(83) Evidence from the antimony tartrate studies outlined above suggests a rapid
dissolution rate of the order of 30 d–1, which is applied here to all Type F forms of antimony.
Extent of binding of antimony to the respiratory tract(84) Evidence from the antimony tartrate studies outlined above suggests that following
the rapid phase of absorption only about 1% of the ILD clears relatively slowly from thelungs. There is no evidence available that clearance of this material is mainly by absorption toblood, as assumed for material in the ‘bound state’. It is therefore assumed that for antimony
the bound state can be neglected, i.e. fb = 0.0.
Table 3-2. Absorption parameter values for inhaled and ingested antimony
Absorption
parameter Absorption fromvaluesathealimentaryfrsr (d–1) ss (d–1) tract, fA

Inhaled particulate materials
Default parameter valuesb,cAbsorption
Type
F
Chloride, tartrate
1
M
Trioxide, all unspecified 0.2
formsdS—
0.01
Ingested materials
All forms
1293
1294
1295
1296
1297
1298
1299
1300
1301
1302
1303
1304
1305
1306
1307
1308
1309
1310
1311
1312
1313
1314

a

b

c

d

30
3

–
0.005

0.05
0.01

3

1x10-45x10-40.05

It is assumed that for antimony the bound state can be neglected, i.e. fb = 0.0. The values of sr for Type F, M
and S forms of antimony (30, 3 and 3 d–1, respectively) are the general default values.
Materials (e.g. antimony chloride) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see text).
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of antimony (0.05).
Default Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

3.2.2. Ingestion(85) No controlled studies on antimony absorption in humans have been carried out,
though an accidental exposure to antimony-containing dust (Rose and Jacobs, 1969)
demonstrated absorption to be less than 0.05. Results from experiments using female rhesus
monkeys suggest that the absorption of Sb administered as tartar emetic (antimony potassium
tartrate) was about 0.3 (Waitz et al, 1965) while comparable studies with rats gave lower
values of about 0.05 for this compound (Moskalev, 1964). Most studies performed on
different chemical forms of Sb(III) and Sb(V) indicated that intestinal absorption was not
usually greater than 0.01 (Rose and Jacobs, 1969; Thomas et al, 1973; Felicetti et al, 1974b),
whereas Gerber et al. (1982) found a value of 0.07 for Sb(III) in pregnant mice. Chertok and32

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1315
1316
1317
1318
1319
1320
1321
1322
1323
1324
1325
1326
1327
1328
1329
1330
1331
1332
1333
1334
1335
1336
1337
1338
1339
1340
1341
1342
1343
1344
1345
1346
1347
1348
1349
1350
1351
1352
1353
1354
1355
1356
1357
1358
1359
1360
1361
1362

Lake (1970) reported that, for dogs fed with 122Sb in debris from a sub-surface nuclear test
site, absorption was at least 0.04. Results obtained by Van Bruwaene et al. (1982) for theexcretion of 124Sb after oral administration as the chloride, compared with data for
intravenous injection, suggested absorption greater than 0.02. Inaba et al. (1984) administered125
Sb to rats, either mixed with blood or biologically incorporated into blood cells andreported absorption of about 0.01 and 0.5, respectively.
(86) In Publication 30 (ICRP, 1981), the recommended absorption values were 0.1 for
antimony in tartar emetic and 0.01 for all other forms. In Publication 69 (ICRP, 1995), avalue of 0.1 was applied to dietary intakes. Because of the variability of the data, a single fAvalue of 0.05 is recommended here for all situations where specific information is notavailable.
3.2.3. Systemic Distribution, Retention and Excretion
3.2.3.1. Summary of the database(87) The biokinetics of antimony in the human body is not well characterized despite along history of therapeutic use of stable antimony and a number of bioassay studies on
workers exposed to known levels of stable antimony in air. Subjects administered antimony
compounds for therapeutic purposes generally have received large masses of antimony
compared with the estimated normal body content. It is uncertain whether the biokinetic data
for these subjects reflect normal biokinetics of antimony, but comparative data for different
masses of administered antimony do not reveal a mass effect on the excretion rate.
(88) Antimony occurs in nature either in the trivalent or pentavalent state, with thetrivalent state being the more common and more stable. Trivalent and pentavalent antimony
initially show different biokinetics after entering the systemic circulation. For example,
Sb(III) is excreted in urine at a lower rate and accumulated by red blood cells at a higher rate
than Sb(V) in the first day or two after intravenous or intramuscular injection. There isevidence of some reduction of Sb(V) to Sb(III) in vivo and convergence of the systemic
biokinetics of these two initial forms over time, but data on the rate and extent of conversionof Sb(V) to Sb(III) are inconsistent.
(89) Information on the time dependent distribution of systemic antimony comes mainly
from animal studies. Some species dependence in the behavior of antimony is indicated. For
example, rats have shown much higher accumulation of antimony in red blood cells (RBC)
than mice, dogs, or human subjects. The collective animal data indicate rapid early loss ofabsorbed or injected antimony in urine and concentration of much of the retained antimony inthe liver, skeleton, and skin or pelt. The longest observed biological half-times for systemic
antimony have varied from several days to a few months. Study periods generally have been
too short to detect any small long-term component of retention.
Human subjects(90) Boyd and Roy (1929) compared the rate of excretion of antimony by patients
following intravenous administration of Sb(III) as antimony sodium tartrate and Sb(V) as
ethylstibamine. Following injection of Sb(III) about 2.5% of the antimony was excreted from
0-24 h, 2% from 24-48 h, and 1% or less from 48-72 h. Following injection of Sb(V) about
19% of the antimony was excreted in urine from 0-2.5 h, 41% from 0-24 h, 6% from 24-48 h,and 1.25% from 48-72 h. Thereafter, daily excretion remained at 1% or less through day 13
following injection. Intramuscular injection of the Sb(V) compound produced a slightly
33

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1363
1364
1365
1366
1367
1368
1369
1370
1371
1372
1373
1374
1375
1376
1377
1378
1379
1380
1381
1382
1383
1384
1385
1386
1387
1388
1389
1390
1391
1392
1393
1394
1395
1396
1397
1398
1399
1400
1401
1402
1403
1404
1405
1406
1407
1408
1409
1410

lower excretion rate over the first two days than intravenous injection of the same compound.
(91) Khalil (1931) examined urine, faeces, sweat, milk, and sputum as routes of excretionof antimony in subjects undergoing treatment with Sb(III) as antimony potassium tartrate or
stibophen. Urine and faeces appeared to be the only significant routes of excretion. During
the 45-d observation period about 45-50% of administered antimony was excreted in urine
and about 3.5% was excreted in faeces.
(92) Goodwin and Page (1943) measured urinary excretion of stable antimony by humansubjects from 1-48 h after intravenous or intramuscular injection of Sb(III) as stibophen or
intravenous injection of Sb(V) as sodium stibogluconate. Cumulative urinary excretion at 24
and 48 h after injection of Sb(III) was 20.4 +/- 2.2% (mean +/- standard deviation) and 23.9+/- 3.6%, respectively, after intravenous injection and 24.0 +/- 9.9% and 26.5 +/- 12.0%,
respectively, after intramuscular injection. A fivefold difference in the mass of antimony
administered intravenously (42.5 mg versus 8.5 mg) had little if any effect on the excretion
rate. Total urinary excretion of antimony over the first 48 h after administration of Sb(V) was
83 +/- 6% of the injected amount. The portion of antimony excreted as Sb(III) afteradministration of Sb(V) was low and variable (1.1-7.6%) over the first 6 h but rose to 50-56%
at 28-48 h, indicating gradual conversion of Sb(V) to S(III) in the body.
(93) Following intravenous infusion of Sb tartar emetic (KSb(III) tartrate) to eight male
African soldiers suffering from schistosomiasis, 21±4% (range 18-23%) of the dose was
excreted in the urine within 72 h (Alves and Blair, 1946).
(94) Bartter et al. (1947) investigated the biokinetics of Sb(III) in seven volunteers
receiving 124Sb tartar emetic by intravenous injection. More than 90% of the injected activity
was removed from blood within 30 min after injection. Thereafter the blood content declined
much more gradually. During the first day urinary and faecal excretion averaged 10.5 +/1.9% and 1.5 +/- 0.4%, respectively, of the administered amount. During the first five days
urinary and faecal excretion averaged 21.2 +/- 4.6% and 4.4 +/- 1.3%, respectively. Urinary
and faecal excretion of antimony measured in one subject over the first 27 d accounted for
66% and 7%, respectively, of the administered amount. The removal half-time from the bodyin this subject was about 14 d between 1 and 27 days after injection. Based on 44 individual
daily measurements of excreta from all seven subjects, the mean daily urinary to faecal
excretion ratio was 6.8 (range 0.6-25.8).
(95) Otto et al. (1947) determined antimony levels in blood plasma, red blood cells, andurine of 14 patients after intramuscular injection of trivalent antimony compounds(anthiolimine or monosodium antimony thioglycollate) or pentavalent antimony compounds(antimony sodium gluconate or ethylstibamine). Trivalent antimony showed five-fold higher
concentrations in red blood cells than plasma within the first 24 h after injection. Pentavalent
compounds showed much lower affinity than trivalent compounds for red blood cells.
Average 24-h urinary excretion of antimony was lower for trivalent compounds (11.4% foranthiolimine and 8.1% for monosodium antimony thioglycollate) than pentavalent
compounds (43% for antimony sodium gluconate and 17% for ethylstibamine).
(96) Abdallah and Saif (1962) reported studies in which 25 male volunteers were given
sodium 124Sb(III)-dimercaptosuccinate (124Sb-DMSA) by intramuscular or intravenous
injection. Following intramuscular injection, cumulative excretion accounted for about 25%of administered 124Sb after 1 d, 50% after 15 d, and 68% after 32 d. Following intravenous
injection, cumulative excretion accounted for about 35% of the administered 124Sb after 1 d
and 63% after 4 d. External measurements indicated relatively high accumulation of activity
in the liver. The liver content peaked about 2 d after injection. Two components of retention
in the liver are indicated by a plot of the measurements. Approximately 80-85% of the peak
34

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content was removed with a half-time of a few days and the remaining 15-20% had a much
longer retention time that could not be quantified over the relatively short observation period.
(97) Taylor (1966) reported measurements of antimony in the urine of workers who had
inhaled SbCl3. The data are too sparse to allow a detailed analysis but indicate rapid
elimination of absorbed antimony in urine.
(98) Rose and Jacobs (1969) reported a case of acute inhalation of a relatively insoluble
form of 124Sb by a worker in a nuclear research facility. The intake could not be estimatedwith much accuracy by whole-body counting during the first day due to surface contaminationof the worker’s body. During the first 10 d after intake the authors estimated total faecal
excretion to be about 1000 times total urinary excretion of 124Sb. The rate of urinary
excretion of 124Sb declined rapidly over the first few days after the incident. In the early
weeks after the incident the effective half-life of 124Sb in the body was approximately 30 d,corresponding to a biological half-time of ~60 d. In later months the effective half-life wasabout the same as the radiological half-life of 124Sb (~60 d), indicating little biologicalremoval of 124Sb from the body. The authors interpreted the data as indicating removal of“transportable material in the tissue” with an effective half-time of 30 d during the early
weeks after the incident and much slower removal of non-transportable material from thelungs at later times.
(99) Rees et al. (1980) measured the time-dependent concentrations of antimony in bloodplasma and urine of human subjects following intravenous injection of Sb(V) as sodium
stibogluconate. The data indicate three phases of removal of antimony from blood plasma,with half-times of 0.2 h (71%), 1.4 h (28%) and 6.9 h (1%). Following intramuscular
injection the plasma clearance from 1 to 24 h appeared to be exponential with a biologicalhalf-time of ~2.5 h. The renal clearance rate of antimony approximated the glomerular
filtration rate. More than 90% of administered antimony was excreted in urine in the first 8 h
after intravenous or intramuscular injection.
(100) Chulay et al. (1988) studied blood clearance of antimony in two patients given Sb(V)as sodium stibogluconate and three patients given Sb(V) as meglumine antimoniate. All
patients were injected intramuscularly with 10 mg Sb/kg daily for 20 d. The two drugs
showed similar biokinetics in blood, with peak blood concentrations appearing about 2 h after
the initial injection. In both cases the blood content of antimony could be described by athree-term exponential model representing an initial absorption phase with a half-time of 0.85
h followed by a rapid elimination phase with a mean half-time of 2 h and a slower phase witha mean half-time of 76 h.
(101) Bailly et al. (1991) reported the case of a woman who attempted suicide by ingestionof an unknown amount of Sb(III) as antimony trisulphide (Sb2S3, stibnite). Only a small
fraction of the intake was absorbed from the gastrointestinal tract. The concentration of
antimony in blood was measured over a period of about 130 h after intake. The bloodconcentration peaked at ~4 h post intake and thereafter decreased bi-exponentially, withestimated biological half-times of ~2.6 h (60%) and 210 h (40%). The urinary excretion rate
peaked about 20 h after intake and declined with a half-time of about 46 h over the next 6 d.
The concentration of antimony in liver bile peaked about 3 h after intake and from 3-60 h
decreased with a half-time of about 12 h. Interpretation of the data for this subject iscomplicated by the fact that efforts were made to remove antimony from the body by forced
diuresis, repeated gastric lavage, and chelation therapy.
(102) Bailly et al. (1991) studied the urinary excretion of antimony in 22 workers
employed in the production of the Sb(V) compounds antimony pentoxide and sodium
antimoniate. The rate of urinary excretion of antimony during an 8-h shift was highly
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correlated with the concentration of antimony in air during the same period, indicating
absorption and rapid removal of a portion of inhaled antimony in urine. Exposure to airborne
antimony at a concentration of 500 μg/m3 was estimated to lead to an increase in urinary
antimony of 35 μg Sb/g creatinine during an 8-h shift.
(103) Kentner et al. (1995) studied occupational exposure to two antimony compounds that
occur in the production of lead batteries: Sb2O3 in the casting of grids, and SbH3 in theformation of lead plates. The concentration of antimony was measured in air in the gridcasting area and formation area and in blood and urine of seven workers from the grid-castingarea and 14 workers from the formation area. Comparisons of the concentrations of antimony
in air and in blood and urine of the workers suggest similar biokinetics of the two forms ofinhaled antimony. At the end of the work shifts the median concentration of antimony in air
was 4.5 (1.18-6.6) μg Sb/m3 in the casting area and 12.4 (0.6-41.5) μg Sb/m3 in the formation
area. The median blood concentrations in pre-shift samples was 2.6 (0.5-3.4) μg Sb/L for the
casting area and 10.1 (0.5-17.9) μg Sb/L for the formation area. The average concentration of
antimony in urine was 3.9 (2.8-5.6) μg Sb/g creatinine for the casting area and 15.2 (3.5-23.4)
μg Sb/g creatinine for the formation area.
(104) Luedersdorf et al. (1987) determined levels of antimony in blood and urine of 109
workers exposed to the oxide of trivalent antimony (Sb2O3) in the glass-producing industry.
Workers were divided into four groups with different tasks and different levels of exposure to
antimony. The concentration ratio of antimony in urine (median value in μg/ml) to antimony
in blood (median value in μg/ml) was 1.9 for all 109 workers and varied from 1.1 to 4.5 forthe four groups.
(105) Liao et al. (2004) determined levels of five metals including antimony in blood andurine of 103 optoelectronic workers. The concentration ratio of antimony in urine (medianvalue in parts per billion) to antimony in blood (median value in parts per billion) was 2.5 forall 103 workers and varied from 2.2 to 4.7 for three different groups of workers with different
tasks and levels of exposure.
(106) The stable antimony content of human tissues has been determined in a number ofoccupationally or non-occupationally subjects (Smith, 1967; ICRP, 1975; Sumino et al.,
1975; Iyengar et al., 1978; Lindh et al., 1980; Gerhardsson et al., 1982; Coughtrey andThorne, 1983). The reported contents of individual tissues as well as relative contents ofdifferent tissues are variable, but the data together with estimates of intake of antimony
suggest the existence of long-term components of retention of antimony in bone and soft
tissues.
Coughtrey and Thorne (1983) estimated on the basis of reported tissue
concentrations that bone typically contains about 55% of the total-body content of stable
antimony. Newer data from Zhu et al. (2010) on the antimony content of tissues from
Chinese males suggest a skeletal content of about 28% of the total body content. Data ofGehardsson et al. (1982) for deceased smelter workers indicate that the total antimony content
of liver typically was an order of magnitude greater than that of the kidneys. This conclusion
is reported by the data of Zhu et al. (2010) for Chinese males.
Animal studies(107) Goodwin and Page (1943) studied urinary excretion of antimony by mice following
subcutaneous, intravenous, or intramuscular injection of one of three Sb(III) compounds(stibophen, KSb-tartrate, or anthiomaline) or one of five Sb(V)- compounds (NaSb-gluconate,stibamine glucoside, neostibosan, urea-stibamine, or stibacetin). For all compounds and all
exposure routes, urinary excretion over the first 48 hours accounted for 50-82% of theadministered antimony.
36

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(108) Brady et al. (1945) reported that in four dogs the urinary excretion of radioactive
Sb(III) over 36 h after intravenous injection with Sb tartar emeric was 14±8% (range 4 -21%).
The urinary excretion in one dog injected intravenously with Sb(III) as sodium antimonyl
xylitol was 13.7% in 36 h.
(109) At four days after intramuscular injection of rats with 122,124Sb as HSbO3, blood andbone contained 2% and 0.9%, respectively, of the injected activity (Durbin, 1960). The liver,kidneys, and muscle each contained 0.1% or less of the injected amount. Urinary excretionaccounted for 96.5% of total excretion over the four-day period.
(110) Djuric et al. (1962) studied the distribution and excretion of 124Sb in rats after
inhalation of an aerosol of 124SbCl3 Two rabbits and one dog were administered intratracheal
doses of the same compound for comparison. Rapid early loss from the rat lung was followed
by slower loss with a half-time on the order of 100 d. The primary site of accumulation ofabsorbed 124Sb in rats was the red blood cells. Such high accumulation in red blood cells was
not evident in the rabbits or dog.
(111) Moskalev (1964) administered 124Sb tartrate emetic to rats by oral or intravenous
administration of 124Sb. The liver and skeleton were found to be important repositories for
antimony over the first 8 d following either route of administration, but the division ofactivity between these two organs depended strongly on the route of administration.
Comparison with earlier results by the same author indicated that the distribution following
intravenous administration also depended strongly on the physicochemical state of antimony
in the initial solution.
(112) In mice receiving 124Sb-KSb tartrate by intraperitoneal injection, about 80% of theadministered amount was excreted the first day and 99% during the first three weeks(Rowland, 1968). The concentration of 124Sb in blood decreased by a factor of ~20 from 15
min to 6 h after injection and by a factor of ~2 from 6 h to 24 h after injection. Loss ofactivity from the liver was slower than from the rest of the body but dropped to 0.5-1% of its
peak value after 21 d.
(113) Thomas et al. (1973) exposed three groups of mice to 124Sb aerosols in a system thatyielded head-only exposures. The aerosols were produced from a starting solution of Sbtartrate but were formed at different temperatures for each group: 100, 500, or 1100 °C. The
activity contained in the material formed at the lowest temperature cleared from the lungs
soon after deposition and deposited primarily in bone, which was estimated to receive a muchhigher radiation dose than the lungs in this case. The activity in the material formed at thetwo higher temperatures was retained in the lungs for a longer period but gradually
accumulated to a large extent in bone, although the lung was estimated to receive a muchhigher radiation dose than bone in this case. In all three groups the portion of the body burden
found in the pelt excluding the head increased from ~7% at 1 d to ~25% at 52 d after
exposure.
(114) Felicitte et al. (1974a) investigated the biokinetics of trivalent and pentavalent 124Sb
over 32 d following inhalation of relatively soluble aerosols by Syrian hamsters. Whole-bodyclearance of both aerosols occurred in two phases. More than 90% of the initial body burden
was eliminated over the first 7 d after exposure. The remaining activity was eliminated with abiological half-time of about 16 d. No significant difference in excretion patterns wasobserved between the two aerosols. Systemic activity was found mainly in liver, skeleton,and skin (shaved pelt). Activity in liver generally was higher after inhalation of the trivalentthen the pentavalent 124Sb, but the opposite pattern was seen for bone. In blood, 124Sb inhaledin the trivalent form was concentrated in the RBC at all sampling times, with maximum RBC
concentration of 6-10 times the plasma concentrations at approximately 24 h after exposure.
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For activity inhaled in the pentavalent form, concentrations were greater in plasma than RBC
in the early hours after exposure, but the RBC to plasma ratio converged over the first day tothat seen for inhaled trivalent 124Sb.
(115) Felicitte et al. (1974b) studied the biokinetics of inhaled 124Sb in groups of beagle
dogs exposed to trivalent 124Sb aerosols formed at different temperatures (100, 500, or 1000
°C). Particle sizes were 1.3, 1.0, and 0.3 μm AMAD, respectively, for aerosols formed atthese three temperatures. Much of the activity inhaled in the aerosol generated at 100 °C
cleared rapidly from the lungs and was excreted in urine at a high rate. Activity inhaled in theaerosols formed at higher temperatures was cleared more slowly from the lungs, and theurinary to faecal excretion rate was much lower at early times than for the aerosol formed at
100 °C. For example, urinary excretion of 124Sb was at least 7 times as great as faecal
excretion over the first 24 h following inhalation of the aerosol formed at 100 °C, comparedwith a urine to faeces ratio of about 0.4 over the same period for the aerosol formed at 500°C. From 1-32 d post exposure the urinary to faecal excretion ratio was not significantly
different for the three aerosols. From 1-21 d post exposure the concentration of 124Sb in RBC
was on average 6.7 times that in plasma. Average long-term biological half-lives for totalbody 124Sb were 100, 36 and 45 d for 124Sb inhaled in aerosols formed at 100, 500, and 1000
°C, respectively. Systemic activity was found mainly in liver, skeleton, and pelt.
(116) Van Bruwaene et al., (1982) studied the urinary and faecal excretion of inorganic
124,125
Sb by lactating cows after oral or intravenous administration. During a 70-d period after
intravenous injection about 51% of the administered amount was excreted in the urine and2.4% was excreted in faeces. Almost 16% of the injected amount was found in tissues at 70
d, but most of this was found in the heart and presumed to have resulted from deposition of
antimony in blood vessels near the injection site as had been observed in an earlier animal
study with antimony. Different systemic distributions were found for the two exposure routes.
Excluding the deposit in the heart, activity retained at 70 d was found mainly in the liver(69% of the body burden), skeleton (7.1%), muscle (7.0%), skin (6.7%), and spleen (6.4%).
At 102 days after oral administration the retained activity was found mainly in the skin (43%of the body burden), skeleton (30%), muscle (10%), and liver (7.3%). The high content of
antimony in liver and spleen following intravenous injection may have been due to uptake
and retention of colloidal antimony.
(117) Bailly et al. (1991) studied the urinary and faecal excretion of Sb(III) by rats after
intraperitoneal or intravenous injection of SbCl3. During the first day, urinary and faecal
excretion accounted on average for about 8.6% and 31%, respectively, of antimony
administered by intraperitoneal injection and 19% and 17%, respectively, of antimony
administered intravenously.
3.2.3.2. Biokinetic model for systemic antimony(118) The structure of the biokinetic model for systemic antimony is shown in Figure 3-1.
Transfer coefficients are listed in Table 3-3. These coefficients are based on data for trivalent
antimony, which has been studied more than pentavalent antimony and which is expected tobe the more frequently encountered form of antimony. For radioisotopes of antimony
entering the systemic circulation as pentavalent antimony, the model is expected tounderestimate the initial rate of biological removal from the body and overestimate
cumulative nuclear transformations in systemic tissues and fluids.

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Figure 3-1. Structure of the biokinetic model for systemic antimony.

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Table 3-3. Transfer coefficients for systemic antimony
From
To
Transfer coefficient(d-1)
PlasmaSmall intestine contents
1.0
PlasmaUrinary bladder contents
12
PlasmaLiver 0
4.0
PlasmaKidneysa
0.3
PlasmaRBC
1.25
PlasmaST075
PlasmaST1
4.35
PlasmaST2
0.1
PlasmaCortical bone surface
1.0
PlasmaTrabecular bone surface
1.0
RBC
Plasma0.0693
Liver 0
Plasma0.3235
Liver 0
Small intestine contents
0.1155
Liver 0Liver 10.0231
Liver 1
Plasma0.0347
Kidneys
Plasma0.231
ST0
Plasma0.693
ST1
Plasma0.0693
ST2
Plasma0.0019Cortical bone surface
Plasma0.03396
Trabecular bone surface
Plasma0.03396
Cortical bone surface
Cortical bone volume0.000693
Trabecular bone surface
Trabecular bone volume0.000693
Cortical bone volume
Plasma0.0000821
Trabecular bone volume
Plasma0.000493
a

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Assigned to “Other kidney tissue” in the generic model for bone-surface-seeking radionuclides.

(119) It is assumed that antimony leaves blood plasma at the rate 100 d-1 (half-time of ~10min) with 75% moving to the fast-turnover soft-tissue compartment ST0, 1.25% to RBC,
12% to the urinary bladder contents, 1% to the contents of the small intestine, 4% to liver(compartment Liver 0), 0.3% to kidneys, 2% to bone surfaces, 0.1% to the slow-turnover softtissue compartment ST2, and the remaining 4.35% to the intermediate-term soft-tissuecompartment ST1. Half of the activity deposited on bone surfaces is assigned to cortical boneand half to trabecular bone. The following removal half-times are assigned: 10 d from RBC
to plasma, 1 d from ST0 to plasma; 10 d from ST1 to plasma; 1 y from ST2 to plasma; 1.5 dfrom Liver 0, with 25% moving to the small intestine contents in bile, 5% moving to thelonger-term liver compartment Liver 1, and 70% returning to plasma; 20 d from Liver 1 toplasma; 3 d from kidneys to plasma; and 20 d from cortical or trabecular bone surface, with98% returning to plasma and 2% moving to the corresponding bone volume compartment.
The transfer coefficients describing the rates of movement from the bone volume
compartments to plasma are the generic turnover rates for cortical and trabecular bone.
(120) The transfer coefficients listed in Table 3-3 yield the following predictions, which
are reasonably consistent with the biokinetic database for antimony summarized above.
There is an initially rapid disappearance of antimony from blood, with only ~15% of
intravenously injected antimony remaining in blood at 30 min and <4% at 1 h after
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administration. This rapid phase is followed by a slow phase of disappearance from blood
due to accumulation and slow release of antimony by RBC and return of antimony fromextravascular spaces to blood. Over the next several days the blood content remains at about
2-3% of the injected amount. The ratio of the concentration of antimony in RBC to that inblood plasma increases to about 5 during the first 24 h after intravenous injection andincreases more gradually over the next few weeks. Antimony is removed from the body
mainly in urine, with urinary losses representing approximately 17% of intravenously injected
antimony after 24 h, 41% after 1 wk, 69% after 1 mo, and 86% after 1 y. The urinary tofaecal excretion ratio based on cumulative excretion is about 7. At equilibrium the ratio of
the concentration of antimony in urine to that in blood is about 2. Most (>75%) antimony
transferred from blood plasma to extravascular spaces following acute input to plasma returns
to plasma in the next few days. The liver initially has a higher concentration than othertissues, but most of the initial liver content is lost over several days. At times greater thanabout one month after intravenous injection the concentration of antimony in the skeleton
exceeds that in the liver. About half the total body content remaining at 1 wk after
intravenous injection is lost over the next 15 d; about half the content remaining at 1 mo islost over the next 25 d; and about half the content remaining at 1 y is lost over the next 2 y.
From 1 wk to 1 mo after intravenous injection the liver content accounts for 5-6% of totalbody antimony. The skeleton content as a fraction of total-body antimony increases fromabout 11% at 1 wk to about 27% at 1 mo. At equilibrium the skeleton contains about half oftotal-body antimony. Based on a constant input to blood of 2 μg of antimony per day fromenvironmental sources (Coughtrey and Thorne, 1983), the model predicts a total-body content
of 7 mg after 10,000 d. This is reasonably consistent with estimates of the total-body content
based on tissue measurements (Coughtrey and Thorne, 1983).
3.2.3.3. Treatment of radioactive progeny(121) Chain members addressed in the derivation of dose coefficients for antimony
isotopes are isotopes of antimony, tellurium, iodine, or xenon. Isotopes of antimony,tellurium, or iodine produced in systemic compartments are assumed to follow thecharacteristic models for these elements (i.e. the models applied in this report to theseelements as parent radionuclides) from their time of production, insofar as application of thisassumption is straightforward. This assumption is sometimes ambiguous due to differences
in model structures for the different elements. That is, the site of production of a radionuclide
may not be clearly identifiable with a specific compartment in its characteristic model. In
such cases a transfer rate from the site of production of the radionuclide to the central bloodcompartment in the radionuclide’s characteristic model has been assigned as described below.
After reaching its central blood compartment, the radionuclide is assumed to behave as
described by its characteristic model.
(122) Tellurium atoms produced at soft-tissue sites in the antimony model that are
ambiguous with regard to the characteristic model for tellurium (ST0, ST1, ST2, Liver 0, andLiver 1) are assumed to be transferred to the central blood compartment of that model(plasma) at the rate 0.0693 d-1 (half-time of 10 d). This is the rate of removal from all soft
tissue compartments in the characteristic model for tellurium. Tellurium produced in RBC isassumed to transfer to plasma at the rate 1000 d-1 (a default rate representing rapid transfer
between compartments). For modeling convenience, tellurium produced in the central bloodcompartment of the antimony model is assigned to the central blood compartment in thetellurium model.
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(123) Iodine atoms are produced at the following sites in the antimony or tellurium models
that are not clearly identifiable with specific compartments of the characteristic model for
iodine: blood compartments, liver compartments, kidneys, thyroid (in the tellurium model),compartments within “Other soft tissue”, and bone compartments. The following rates oftransfer from these compartments to the blood iodide pool of the characteristic model for
iodine are assigned: liver compartments or kidneys, 100 d-1 (the rate of loss from the liver
iodide and kidney iodide compartments in the characteristic model for iodine); bloodcompartments (excluding central blood compartments, as indicated below) 1000 d-1; Other
soft tissue or bone surface compartments, 330 d-1 (the highest transfer coefficient to blood in
the characteristic model for iodine); thyroid, 36 d-1 (the transfer coefficient from the thyroid
iodide pool to the blood iodide pool in the characteristic model for iodine); trabecular andcortical bone volume compartments, the reference rates of trabecular and cortical boneturnover. For modeling convenience, iodine atoms produced in the central blood pools of theantimony and tellurium models are assigned to the blood iodide pool in the characteristic
model for iodine.
(124) A generic biokinetic model is applied in this report to xenon isotopes produced bydecay of a radionuclide in systemic compartments. Xenon produced in bone is assumed totransfer to blood at the rate 100 d-1 if produced in bone surface and 0.36 d-1 if produced inbone volume. These rates are taken from the model for radon introduced in ICRP Publication
67 (1993) and applied in this report to radon produced in bone surface and non-exchangeablebone volume, respectively, by decay of a radium isotope. Xenon produced in a soft-tissuecompartment is assumed to transfer to blood with a half-time of 20 min. Xenon produced in
the central blood compartment in the model for antimony, tellurium, or iodine is assigned tothe blood compartment of the xenon model. Xenon produced in any other blood compartmentin the antimony, tellurium, or iodine model is assumed to be transferred to blood in the xenon
model at the rate 1000 d-1. Xenon entering the blood compartment of the xenon model orproduced in that compartment is assumed to be removed from the body (exhaled) at the rate
1000 d-1. Recycling of xenon to tissues via arterial blood is not depicted explicitly in thismodel for xenon as a daughter radionuclide but is considered in the assignment of the halftimes in tissues. The model is intended to yield a conservative average residence time ofxenon atoms in the body after their production in systemic pools.
3.3.

(125) 124 Sb may be monitored through Whole Body Counting and/ or Urine bioassay.
IsotopeMonitoring
Technique124

Urine Bioassay
Lungmeasurement
Whole
Body γ-ray spectrometry
Counting

124

124

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Individual monitoring

Sb
Sb
Sb

MethodMeasurementof Typical
Detection
Limit
1 Bq/L
γ-ray spectrometry
γ-ray spectrometry 9Bq*
30 Bq

Achievabledetection limit
0.02 Bq/L

12 Bq∗ Lung monitoring of 124Sb is not generally used in routine monitoring of workers. Monte Carlo program VisualMonte Carlo was used to simulate the photon emission, to calculate the calibration factor for the geometry andradionuclide, and to calculate the minimum detectable activity (MDA) in the lung. (Hunt et al, 2012)(126) 125 Sb may be monitored through Whole Body Counting and/ or Urine bioassay.
42

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1716

Isotope
125
125

1717
1718
1719
1720
1721
1722
1723
1724
1725
1726
1727
1728
1729
1730
1731
1732
1733
1734
1735
1736
1737
1738
1739
1740
1741
1742
1743
1744
1745
1746
1747
1748
1749
1750
1751
1752
1753
1754
1755
1756
1757
1758
1759

Sb
Sb

Monitoring
Technique

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
6 Bq/L
γ-ray spectrometry
Whole
Body γ-ray spectrometry 100 Bq
Counting

Achievabledetection limit
0.1 Bq/L
40 Bq

References
Abdallah, A., Saif, M., 1962. Tracer studies with antimony-124 in man. In: Wolstenholme, G.E.W.
and O’Connor, M. (Eds.) Bilharziasis. Churchill, London, pp. 287-309.
Alves, W., Blair, D.M., 1946. Schistosomiasis. Intensive treatment with antimony. Lancet, 247, 9-12.
Bailly, R., Lauwerys, R., Buchet, J.P., Mahieu P., Konings, J., 1991. Experimental and human studies
on antimony metabolism: their relevance for the biological monitoring of workers exposed toinorganic antimony, Br. J. Ind. Med. 48, 93–97.
Bartter, F.C., Cowie, D.B., Most, H., Ness, A.T., Forbush, S., 1947. The fate of radioactive tartar
emetic administered to human subjects. 1. Blood concentrations and excretion following
single and multiple intravenous injections. Amer. J. Trop. Med., 27, 403-416.
Boyd, T.C., Roy, A.C., 1929. Observations on the excretion of antimony in the urine. Indian J. Med.
Res., 17, 94-108.
Brady, F.J., Lawton, A.H., Cowie, D.B., Andrews, H.L., Ness, A.T., Ogden, G.E., 1945. Localizationof trivalent radioactive antimony following intravenous administration to dogs infected withdirofilaria immitis. Amer. J. Trop. Med., 25, 103-107.
Brahmachari, U.N., Chaudhury, S.C., Das, J., Sen, P.B., 1924. Chemotherapy of antimonial
compounds in Kala-azar infection. VIII. Quantitative studies in excretion of antimony (tartar
emetic and urea stibamine). Ind. J. Med. Res., 11, 829-838.
Chertok, R.J., Lake, S., 1970. Availability in the dog of radionuclides in nuclear debris from thePlowshare excavation Cabriolet. Health Phys., 19, 405-409.
Chulay, J.D., Fleckenstein, L., Smith, D.H., 1988. Pharmacokinetics of antimony during treatment ofvisceral leishmaniasis with sodium stibogluconate or meglumine antimoniate. Trans. Roy.
Soc. Trop. Med. Hyg., 82, 68.
Coughtrey, P.J., Thorne, M.C., 1983. Antimony. In: Radionuclide distribution and transport interrestrial and aquatic ecosystems, Vol. 3. Rotterdam, Balkema, A.A., pp. 263-304.
Djuric, D., Thomas, R.G., Lie, R., 1962. The distribution and retention of trivalent antimony in the rat
following inhalation. Int. Arch. Gewerbepathol. Gewerbehyg., 19, 529-545.
Durbin, P.W., 1960. Metabolic characteristics within a chemical family. Health Phys., 2, 225-238.
Felicetti, S.A., Thomas, R.G., McClellan, R.O., 1974a. Retention of inhaled antimony-124 in the
beagle dog as a function of temperature of aerosol formation. Health Phys., 26, 525–531.
Felicetti, S.A., Thomas, R.G., McClellan, R.O., 1974b Metabolism of two valence states of inhaled
antimony in hamsters. Amer. Ind. Hyg. Assoc. J., 35, 292–300.
Garg, S.P., Singh, I.S., Sharma, R.C., 2003. Long term lung retention studies of 125Sb aerosols inhumans. Health Phys., 84(4), 457–468.
Gerber, G.B., Maes, J., Eykens, B., 1982. Transfer of antimony and arsenic to the developing
organism. Arch. Toxicol. 49, 159-168
Gerhardsson, L., Brune, D., Nordberg, G.F., Wester, P.O., 1982. Antimony in lung, liver and kidney
tissue from deceased smelter workers. Scand. J. Work Environ. Health 8(3), 201-8.
Goodwin, L.G., Page, J.E., 1943. A study of the excretion of organic antimonials using apolarographic procedure. Biochem. J. 37, 198-209.

43

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1760
1761
1762
1763
1764
1765
1766
1767
1768
1769
1770
1771
1772
1773
1774
1775
1776
1777
1778
1779
1780
1781
1782
1783
1784
1785
1786
1787
1788
1789
1790
1791
1792
1793
1794
1795
1796
1797
1798
1799
1800
1801
1802
1803
1804
1805
1806
1807
1808
1809
1810

Groth, D.H., Stettler, L.E., Burg, J.R. Busey, W.M., Grant, G.C., Wong, L.J., 1986. Carcinogenic
effects of antimony trioxide and antimony ore concentrate in rats. Toxicol. Environ. Health18, 607–626.
IARC, 1989. Antimony trioxide and antimony trisulfide. Volume 47, 291–305. IARC Monographson the Evaluation of Carcinogenic Risks to Humans. IARC, Lyon, France.
ICRP, 1975. Report of the Task Group on Reference Man, ICRP Publication 23. Pergamon Press,
Oxford.
ICRP, 1981. Limits on Intakes of Radionuclides for Workers. ICRP Publication 30, Part 3. Oxford.
Ann. ICRP 6, (2/3).
ICRP, 1993. Age-dependent Doses to Members of the Public from Intake of Radionuclides: Part 2,
Ingestion dose coeffcients . ICRP Publication 67. Pergamon Press, Oxford. Ann. ICRP 23,(3/4).
ICRP, 1995. Age-dependent Doses to Members of the Public from Intake of Radionuclides, Part 3,
Ingestion dose coefficients, ICRP Publication 69. Ann. ICRP 25(1).
Inaba, J., Nishimura, Y., Ichikawa, R., 1984. Studies on the metabolism of antimony-125 in the rat.
NIRS-N-49 (National Institute of Radiological sciences, Chiba, Japan). pp.81-83.
Iyengar, G.V., Kollmer, W.E., Bowen, H.J.M., 1978. The elemental composition of human tissues
and body fluids: A complication of values for adults. Verlag Chemic, New York.
Kentner, M., Leinemann, M., Schaller, K.H., Weltle, D., Lehnert, G., 1995. External and internal
antimony exposure in starter battery production, Int. Arch. Occup. Environ. Health 67, 119–
123.
Khalil, M.B., 1931. The specific treatment of human schistosomiasis (Bilharzias) with specialreference to its application on a large scale. Arch. Schiffs Trop. Hyg. 35 (Supp. 2), 1-128.
Liao, Y-H., Yu, H-S., Ho, C-K., Wu, M-T., Yang, C-Y., Chen, J-R., Chang, C-C., 2004. Biological
Monitoring of Exposures to Aluminium, Gallium, Indium, Arsenic, and Antimony inOptoelectronic Industry Workers. J. Occ. Env. Med., 46(9), 931-936.
Lindh, U., Brune, D., Nordberg, G., Wester, P., 1980. Levels of antimony, arsenic, cadmium, copper,lead, mercury, selenium, silver, tin and zinc in bone tissue of industrially exposed workers.
Sci. Total Environ., 16, 109-116.
Luedersdorf, R., Fuchs, A., Mayer, P., Skulsuksai, G., Schacke, G., 1987. Biological assessment of
exposure to antimony and lead in the glass-producing industry. Int. Arch. Occup. Environ.
Health., 59(5), 469-74.
McCallum, R.I., 1963. The work of an occupational hygiene service in environmental control. Ann.
Occup. Hyg., 6, 55–64.
McCallum, R.I., Day, M.J., Underhill, J., Aird, E.G.A., 1971. Measurement of antimony oxide dust in
humans lungs in vivo by X-ray spectrophotometry. Inhaled Particles III, Vol. 2, Proceedingsof an International Symposium Organised by the British Occupational Hygiene Society,London, 14 – 23 September 1970, pp. 611–619, (Ed. Walton, W.H.) Unwin Brothers Limited,
The Gresham Press, Old Woking, Surrey, England.
Moskalev, Y., 1964. Experiments dealing with distribution of antimony-124 and tellurium-127. AECtr-7590, pp.63-72.
Newton, P.E., Bolte, H.F., Daly, I.W., Pillsbury, B.D., Terrill, J.B., Drew, R.T., Ben-Dyke, R.,
Sheldon, A.W., Rubin, L.F., 1994. Subchronic and chronic inhalation toxicity of antimony
trioxide in the rat. Fund. Appl. Tox., 22, 561–576.
Otto, G.F., Maren, T.H., Brown, H.W., 1947. Blood levels and excretion rates of antimony in persons
receiving trivalent and pentavalent antimonials. Am. J. Hyg., 46, 193-211.
Rees, P.H., Keating, M.I., Kager, P.A., Hockmeyer, W.T., 1980. Renal clearance of pentavalent
antimony (sodium stibogluconate). Lancet 2, 226-229.
Rose, E., Jacobs, H., 1969. Whole-body counter and bioassay results after an acute antimony-124
exposure. In: Handling of Radiation Accidents, International Atomic Energy Agency,
Vienna. IAEA-SM-119/30. pp. 589-600.

44

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
1811
1812
1813
1814
1815
1816
1817
1818
1819
1820
1821
1822
1823
1824
1825
1826
1827
1828
1829
1830

Rowland, H.A.K., 1968. Stibokinetics III: Studies on mice with 124Sb-labelled potassium antimony
tartrate. Tissue concentrations: Excretion. Trans. Roy. Soc. Trop. Med. Hyg., 62, 795-800.
Smith, H., 1967. The distribution of antimony, arsenic, copper and zinc in human tissue. J. Forensic
Sci. Society, 7, 97-102.
Sumino, K., Hayakawa, K., Shibata, T., Kitamura, S., 1975b. Heavy metals in normal Japanese
tissues. Arch. Environ. Health, 30, 487-494.
Taylor, P.J., 1966. Acute intoxication from antimony trichloride. Brit. J. Indust. Med., 23, 318-321.
Thomas, R.G., Felicetti, S.W., Luchino, R.V., McClellan, R.O., 1973. Retention patterns of antimony
in mice following inhalation of particles formed at different temperatures. Proc. Soc. Exp.
Biol. Med., 144, 544-550.
Van Bruwaene, R., Gerber, G.B., Kirchmann, R., Colard, K., 1982. Metabolism of antimony-124 inlactating dairy cows. Health Phys., 43, 733-738.
Waitz, J.A., Ober, R.E., Meisenhelder, J.E., Thompson, P.E., 1965. Physiological disposition of
antimony after administration of 124Sb-labelled tartar emetic to rat, mice and monkeys, andthe effects of tris (p-aminophenyl) carbonium pamoate on this distribution. Bull. WHO 33,
537-546.
Zhu, H., Wang, N., Zhang, Y., Wu, Q., Chen, R., Gao, J., Chang, P., Liu, Q., Fan, T., Li, J., Wang, J.
2010. Element contents in organs and tissues of Chinese adult men. Health Phys., 98, 61-73.

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1831
1832
1833
1834
1835
1836
1837
1838
1839
1840
1841
1842
1843
1844
1845

4.
4.1.

Chemical Forms in the Workplace(127) Tellurium is a semi-metal or metalloid, which occurs mainly in oxidation states –II,
II, IV and VI. Tellurium is in the same chemical series as sulphur and selenium and forms
similar compounds. The two anionic forms are known as tellurates (TeO42- or TeO66-).
(128) Tellurium may be encountered in industry in a variety of chemical forms, including
elemental vapour or solid forms, oxides, chlorides, but also as tellurides.
(129) Tellurium-132 is a fission product which is important in the first few days after acriticality accident.
Table 4-1. Isotopes of tellurium addressed in this report
Isotope
Te-114
Te-116
Te-117
Te-118
Te-119
Te-119m
Te-121
Te-121m
Te-123Te-123m
Te-125m
Te-127
Te-127m
Te-129aTe-129m
Te-131aTe-131ma
Te-132aTe-133Te-133ma
Te-134

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1856
1857
1858

Tellurium (Z = 52)aPhysical half-life
15.2 m2.49 h62 m
6.00 d16.05 h4.70 d
19.16 d154 d
6.00E+14 y
119.25 d
57.40 d9.35 h109 d69.6 m33.6 d25.0 m30 h
3.204 d12.5 m55.4 m41.8 mDecay mode
EC, B+
EC, B+
EC, B+EC
EC, B+
EC, B+EC
IT, ECEC
IT
IT
BIT, BBIT, BBB-, IT
BBB-, ITB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides
are given on accompanying electronic disk.

4.2. Routes of Intake
4.2.1. Inhalation(130) A few experimental studies of the behaviour of radio-labelled tellurium (i.e. tracer
level) following deposition in the respiratory tract have been identified in the literature. Some
information is also available from measurements following inadvertent intakes of irradiatedtellurium oxide, from studies of tellurium-132 inhaled by people after the Chernobyl accident,
and from toxicology studies of stable tellurium compounds.

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1859
1860
1861
1862
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1900
1901
1902
1903
1904
1905
1906

Classification of gases and vapours, absorption Types and parameter values(131) Absorption parameter values and Types, and associated fA values for gas and vapour
forms of tellurium are given in Table 4-2 and for particulate forms in Table 4-3. Common
forms of tellurium (e.g. dioxide) are solids at room temperature. Exposures to gas or vapour
forms of tellurium are therefore probably relatively unusual compared to exposures toparticulate forms, and it is therefore proposed here that particulate form should be assumed in
the absence of specific information.
(a) Gases and vapours(132) Accidental inhalation by two men of tellurium in the form of hexafluoride gas andpossibly also tellurium esters was reported by Blackadder and Manderson (1975). However,
the information reported related mainly to clinical signs and symptoms. Insufficient
information is available to estimate the fraction deposited, or the rate of absorption.
Tellurium in gas and vapour forms are assigned the default behaviour for gases and vapours:
100% total deposition (20% ET2, 10% BB, 20% bb and 50% AI) and Type F absorption(Table 4-2).
(b) Particulate aerosols
Tellurium chloride(133) Dobryakova (1970) followed the biokinetics of 127Te for 14 days after administrationof tellurium chloride to rats by intratracheal instillation. There was rapid absorption from thelungs, but the rate decreased with time. About 40% of the initial lung deposit (ILD) was
absorbed at 30 minutes and 70% ILD at 1 day. Subsequent clearance was slow and mainly
faecal, with about 6% ILD remaining in the lungs at 14 d. Parameter values estimated here
were fr ~0.7, and sr of the order of 50 d–1, but decreasing with time, and assignment to Type F.
Elemental tellurium(134) Geary et al. (1978) investigated the toxicological effects up to 180 days afteradministration of tellurium to rats by intratracheal instillation. No quantitative information on
the biokinetics was reported. However, pigmentation and effects in the lungs and other organs
indicate that the tellurium was not absorbed rapidly and completely, but that significant
absorption did take place, indicative of Type M rather than Type F or S behaviour.
Tellurium dioxide (TeO2)(135) Fehér (1976) followed whole-body retention of 123mTe for up to 45 days after
intratracheal instillation of irradiated TeO2 into rats. The high thyroid uptake of 131I at 1 day
indicated correspondingly rapid (Type F) dissolution of the TeO2 to release the 131I.
(136) Fehér and Andrási (1977) followed whole-body retention of 123mTe for up to 95 days
after intake by 10 workers accidentally contaminated with TeO2 irradiated for the productionof 131I. Retention fit a two-component exponential function, with about 75% and 25%
retained with effective half-times of about 12 and 70 days respectively. The authorsinterpreted the results on the basis that the retained activity was homogeneously distributed in
the body, assuming rapid dissolution (Type F).
(137) Geary et al. (1978) investigated the toxicological effects up to 180 days afteradministration of tellurium dioxide to rats by intratracheal instillation. No quantitative
information on the biokinetics was reported. However, pigmentation and effects in the lungs
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1907
1908
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1910
1911
1912
1913
1914
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1917
1918
1919
1920
1921
1922
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1927
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1930
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1935
1936
1937
1938
1939
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1942
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1944
1945
1946
1947
1948
1949
1950
1951

and other organs indicate that the tellurium was not absorbed rapidly and completely, but thatsignificant absorption did take place, indicative of Type M rather than Type F or S behaviour.
Cadmium telluride (CdTe)(138) As part of a toxicological study, Morgan et al. (1997) measured the concentrations of
cadmium and tellurium in lungs and other tissues up to 28 days after administration of
cadmium telluride to rats by intratracheal instillation. The lung concentrations of bothelements at 28 days was about 30% of that at 1 day, and was accompanied by significant
increases in concentrations in extrapulmonary tissues, giving assignment to Type M.
Unspecified compounds(139) Balonov et al. (2003) summarised the results of in vivo measurements made 4 – 8
days after the Chernobyl accident on 65 people evacuated from Pripyat 1.5 d after theaccident. Tellurium-132 activity was measurable in 56 persons, and in 28 of them withrepeated lung measurements it declined with a half time of 2.5±0.2 d. Taking account of the132
Te decay half-life of 3.3 d gives a lung clearance half time of about 10 d, and acorresponding clearance rate of 0.07 d–1. During the period of measurements the particle
clearance rate from the lungs predicted by the HRTM is about 0.01 d–1, suggesting that mostof the observed clearance is due to absorption to blood, at a rate (ss) of about 0.06 d–1. Since
the lung measurements started a few days after intake, they do not on their own enable anestimate to be made of the fraction that dissolved rapidly. However, measurements were also
made of 132I in the thyroid, which was considered to originate mainly from 132Te deposited thelungs. The mean ratio of 132I activity in thyroid to that of 132Te in lungs was 0.2, but withconsiderable variation between individuals (range 0.07 to 0.6) (Balonov et al, 2003). Analysis
was carried out here to make an estimate of fr based on this ratio. It was assumed that sr = 100
d–1 (default); ss = 0.06 d–1 (see above) and fA = fr * 0.3 (the default assumption for inhaledmaterials, see footnote c to Table 4-3, the fractional uptake in the alimentary tract value foringested soluble forms of tellurium being 0.3). This gave a central estimate for fr of about
0.3, but with a range similar to that of the ratio of 132I activity in thyroid to that of 132Te inlungs above. Thus the results are consistent with assignment to default Type M, although they
indicate faster absorption than assumed by default. Given the uncertainties involved, specificparameter values are not recommended here for tellurium accidentally released from a nuclear
reactor.
Rapid dissolution rate for tellurium(140) Evidence from the tellurium chloride study outlined above suggests a rapid
dissolution rate of the order of 50 d–1, which is applied here to all forms of tellurium.
Extent of binding of tellurium to the respiratory tract(141) Evidence from the tellurium chloride study outlined above suggests that following
the rapid phase of absorption about 6% of the ILD clears relatively slowly from the lungs.
There is no evidence available that clearance of this material is mainly by absorption to blood,
as assumed for material in the ‘bound state’. It is therefore assumed that for tellurium thebound state can be neglected, i.e. fb = 0.0.

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1952
1953
1954

Table 4-2. Deposition and absorption for gas and vapour compounds of tellurium

Chemical form/origin
All unspecified compounds
1955
a
1956
1957
1958
1959
1960
1961
1962

Percentage deposited (%)a
Total
ET1
ET2
BB
b
100
0
20
10

bb
20

AI
50

Percentage deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in, or
react with, the surface lining. The default distribution between regions is assumed: 20% ET2, 10% BB, 20% bb
and 50% AI.

Table 4-3. Absorption parameter values for inhaled particulate forms of tellurium andfor ingested tellurium
Absorption parameter valuesa
Inhaled particulate materials
Default parameter valuesb,cAbsorption
Assigned forms
TypeF
Tellurium chloride, tellurium
dioxideM
Elemental
tellurium,
cadmium
telluride,allunspecified formsd
S—frsr (d–1)

ss (d–1)

Absorption
from the GI
tract, fA

1

50

–

0.3

0.1

50

0.005

0.03

0.001

50

1x10-43x10-4

Ingested materials
All forms
1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
1973
1974
1975
1976
1977
1978
1979
1980
1981
1982
1983
1984

Absorption
Type
fA
F
0.3

a

b

c

d

0.3

It is assumed that for tellurium the bound state can be neglected i.e. fb = 0. The values of sr for Type F, M and
S forms of tellurium (50 d–1) are element-specific.
Materials (e.g. tellurium chloride) are listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see text).
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of tellurium (0.3).
Default Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

4.2.2.

Ingestion(142) Kron et al. (1991) studied the renal excretion of stable tellurium by healthy
volunteers after oral administration of Te as sodium tellurate (TeO3), sodium tellurite (TeO2)
and metallic colloid. The calculated fractional absorption values were 0.23±0.09 in 4
volunteers ingesting Na tellurate, 0.21 in a single volunteer ingesting tellurite, and 0.10±0.04
in 3 volunteers ingesting metallic tellurium. Since the main chemical form of tellurium infission products is sodium tellurite, Kron et al. (1991) proposed that a fractional absorption
value of 0.25 should be applied for radiological protection purposes.
(143) Experimental data from several animal species including rats, guinea pigs, rabbits,
dogs, sheep and cows gave absorption values in the range 0.2 - 0.5 for water soluble tellurites

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1985
1986
1987
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1989
1990
1991
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1993
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1996
1997
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2000
2001
2002
2003
2004
2005
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2010
2011
2012
2013
2014
2015
2016
2017
2018
2019
2020
2021
2022
2023
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2031

(TeO2) and about 0.1 - 0.25 for tellurates (Barnes et al., 1955; Venugopal and Luckey, 1978;
Hollins, 1969; De Meio and Henriques, 1947; Mullen and Stanley, 1974; Taylor, 1996).
Chertok and Lake (1970) argued on the basis of absorption studies on dogs that tellurium
radionuclides contained in nuclear debris might be unavailable for absorption across theintestinal wall.
(144) In Publication 30 (ICRP, 1979), an absorption value of 0.2 was recommended. A
value of 0.3 was adopted in Publication 67 (ICRP, 1993) for intakes in food. The data do notsupport the use of different values for workers and public and therefore an fA value of 0.3 isused here.
4.2.3. Systemic Distribution, Retention and Excretion
4.2.3.1. Summary of the database(145) The biokinetics of tellurium in the human body is not well characterized. There are
only a few data for human subjects, mainly bioassay measurements following accidental
exposure in the workplace. A number of studies deal with the toxicological issues oftellurium incorporation and related side-effects, mainly the occurrence of a sour garlic odour
on the breath and in the urine, sweat and excrement resulting from occupational exposure totellurium. This odour seems to be due to the presence of tiny amounts of dimethyl telluride.
Summary of data for human subjects(146) Schroeder et al. (1967) estimated the content of tellurium in several human tissues
and calculated that the total amount in the body was approximately 600 mg, which would
make tellurium one of the most abundant trace elements in the body. The largest amount was
found in bone (90%), with much lower amounts in muscle (3%), liver (1.2%) and probably infat (3%). The amount found in kidney was approximately 3% of that in liver. The
concentration in blood serum amounted to 1.07±0.12 mg⋅L-1 (i.e. 0.17%⋅L-1), and that inunwashed erythrocytes to 1.95 mg⋅L-1. However, the values for blood may be unreliable due
to analytical problems (Nason and Schroeder, 1967) and were not confirmed by later studies.
Van Montfort et al. (1979), for example, found concentrations in blood of unexposed subjects
to range between 0.15 and 0.3 µg⋅L-1.
(147) Fehér and Andrási (1977) presented the results of a study where an irradiated andcooled suspension of TeO2-131I was administered to two volunteers. The whole-bodyretention of tellurium in the first few days after administration was described with a biexponential function with effective half-times of 0.7 d (75%) and 10 d (25%). These data areconsistent with the whole-body retention measured in ten persons occupationallycontaminated with radiotellurium. For these persons no information was available on fast
clearance, due to the lack of measurements immediately after the accident, but measurements
at later times allowed the determination of longer-term retention components with effective
half lives of 11 d (75%) and 45 d. The combined findings of the experimental study and thefollow-up of the occupationally exposures suggest that whole body retention can be describedby a three-exponential function, with biological half lives of 0.7 d (70%), 12 d (23 %) and 72
d (7 %).
(148) Kron et al. (1991) studied urinary excretion in five healthy volunteers after oral
administration of tellurium in different forms (altogether 12 investigations): tellurite(Na2TeO4), tellurate (Na2TeO3), metallic form, and intrinsically bound in cress (Lepidium

50DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2032
2033
2034
2035
2036
2037
2038
2039
2040
2041
2042
2043
2044
2045
2046
2047
2048
2049
2050
2051
2052
2053
2054
2055
2056
2057

sativum). Cress was consumed both with and without oil and vinegar dressing. The three-day
urinary excretion varied between 3 and 25%. It was higher for tellurate (9 to 25%) than for
tellurite (less than 8%) or metallic tellurium (4 to 9%). After ingestion of tellurium with cress,
the amount excreted over three days ranged between 6 and 16%, and was reduced to 3% whendressing was added. For tellurate and metal tellurium most of the excretion occurred in thefirst 24 h after administration, whereas for cress and tellurite the excretion curve was delayed.
For cress this delay presumably indicates a slower absorption of tellurium bound in organic
matter as compared to the aqueous solutions. For tellurite the authors assumed a higher
retention in the body for this compound as compared to tellurate as an explanation for the
lower and slower excretion.
Summary of data from animal studies(149) DeMeio and Henriques (1947) administered radioactive tellurite to rabbits, rats anddogs and measured the tissue distribution (Table 4-4) and excretion pathways. In rabbits andrats elevated concentrations were measured in kidneys, spleen, heart and lungs, and lower
concentrations were found in the liver. In rats the tissue concentrations dropped considerably
after one hour. Concentrations in blood averaged 25±4%⋅L-1 at day 1 after intravenous
injection in rabbits and 610±390%⋅L-1 in rats at thirty minutes after intraperitoneal
administration. In dogs the values dropped from 21±12%⋅L-1 at 1 hour to 6.9±2.5%⋅L-1 at 1day. About 20 to 23% of tellurite injected intravenously into female dogs was excreted in theurine over 5-6 days, the greatest portion in the first two-three hours. Finally, the authors
concluded that less than 1/1000th of the amount of radioactive tellurite injected into rabbits
was excreted via the expired air during the 24 hr following administration. On the basis of theobserved excretions, the authors argue that about 60% of tellurium injected into dogs
remained in their body after 5-6 days.
Table 4-4. Distribution (%/organ) of radiotellurium activity
following injectiona
Organ
Kidney
Liver
Lung
Heart
SpleenRabbitsb
11.6±3.2
6.6±1.3
1.4±0.5
0.66±0.38
0.28±0.08

Ratsc
6.14±1.90
6.43±0.60
0.73±0.12
0.46±0.15
0.72±0.05

Ratsd
0.33
0.33
0.02
0.02
0.03

a

From DeMeio and Henriques (1947).
Intravenous administration. Values are means for up to six animals each and refer toabout 1 day after administration.
cIntraperitoneal administration. Values are means for up to three animals each andrefer to about 0.5 h after administration.
dIntraperitoneal administration. Values are for only one animal and refer to about 1
day after administration.
b

2058
2059
2060
2061
2062
2063
2064
2065

(150) Barnes et al. (1955) administered 132Te orally to rats and guinea pigs and determinedthe distribution of tellurium in the body at 3-4 days (Table 4-5). About 5.5% and 6.5% was
excreted in the urine over 4 days by the guinea pigs and rats, respectively. Fecal excretion
plus activity present in the gut amounted to about 93% in the guinea pigs and 80% in the rats.
In further experiments, a tellurium solution was injected intravenously into rats, guinea pigs,
mice and one rabbit to follow the blood kinetics and investigate the partition between whole
blood and plasma. In general, retention in the blood of mice, guinea-pigs and the rabbit was

51

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2066
2067
2068
2069
2070
2071
2072
2073

low (at day 1, 0.5 % in the mice, about 1% in the guinea pigs and 3.2% in the rabbit), whereas
in the rats blood retention ranged from 22 to 32%. The biological half-life in the rat was about
seven days. Tellurium in the blood appeared to be contained completely in the plasma inguinea pigs and mice, and only a small portion was bound to the corpuscles in the rabbit. By
contrast, tellurium activity in the blood of rats was significantly higher than in plasma,suggesting that the rat is unique in retaining tellurium within the red cells. Tellurium in the
rabbit's plasma and in the rats' corpuscles was shown to be protein-bound.
Table 4-5. Distribution (%/organ) of 132Te activity following oral
administrationa
Organ
KidneyLiver
Skeleton
Pelt
Carcass
Thyroid
Blood removed
a

2074
2075
2076
2077
2078
2079
2080
2081
2082
2083
2084
2085
2086
2087
2088
2089
2090
2091
2092
2093
2094

Guinea pigs
0.52±0.06
0.73±0.22
0.54±0.08
0.29±0.02
0.35±0.10
0.01±0.005
0.03±0.01

Rats
1.20±0.08
1.13±0.32
0.77±0.03
0.80±0.21
1.94±0.85
0.01±0.005
3.60±0.20

From Barnes et al. (1955). Values are means for two animals each and refer to 3-4 days
after administration.

(151) Casey et al. (1963) administered a mixture of radionuclides of tellurium and iodine
to lactating sheep and found that the transfer to milk was very low (two to three orders ofmagnitude less than for iodine). Retained tellurium was found mainly in the liver, kidney,lungs. The highest concentration was found in the thyroid, but the total content of the thyroid
was small due to its small mass.
(152) Wright and Bell (1966) compared the metabolism of tellurium in sheep and swine.
Five animals of each species were orally administered 127mTe as Na2TeO3 via a stomach tube,
and five more animals received the same compound via injection into the jugular vein. The
blood content of 127mTe in the sheep was very low (less than 0.25% of the administered dose)
after oral administration. Intravenously injected tellurium was cleared readily from plasma(10% was retained after 2 hr and 2% after 5 d), and only a small portion was recovered in thecell fraction. In swine the peak concentration in whole blood occurred at approximately 30
hours after oral administration, at which time nearly all the 127mTe was in the corpuscular
fraction. Clearance of intravenously administered tellurium from plasma was similar to thatobserved in the sheep, but the corpuscular fraction rose with time (up to 3% at 5 d). The
whole blood clearance after iv-administration could be described in terms of two components:
a fast component with a biological half-time of about 10 h and a slower component with ahalf-time of several days. The total organ content at 5 days after intravenous administration is
given in Table 4-6. No information was given about skeleton or thyroid.

52

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

Table 4-6. Distribution of 132Te 5 d after intravenous administration(% of administered activity)
Organ
Kidney
Liver
Lung
Heart
Spleen
a

2095
2096
2097
2098
2099
2100
2101
2102
2103
2104
2105
2106
2107
2108
2109
2110
2111
2112
2113
2114
2115
2116
2117
2118
2119
2120
2121
2122
2123
2124
2125
2126
2127
2128
2129
2130
2131

Sheep
7.14±0.27
7.95±0.47
1.38±0.02
0.81±0.35
0.16±0.01

Swine
2.08±0.33
7.08±0.33
1.48±0.13
0.29±0.04
0.37±0.06

From Wright and Bell (1966). Values presented are the average of five subjects each andrefer to 5 days after administration.

(153) Sheep as well as swine excreted about 11% of the injected 127mTe in the faeces and
34% in the urine over five days. About two-thirds of the urinary excretion occurred in the first
24 h. After oral administration, sheep excreted 75% in the faeces and 20% in the urine. Swine
excreted 70% in the faeces and 19% in the urine, mostly on the second day.
(154) Hollins (1969) studied the metabolism of 127mTe as tellurous acid in rats. The wholebody retention after intraperitoneal injection could be described as a bi-exponential function
with half-times of 0.8 d (49%) and 13 d (51%), respectively. After oral administration 84%
was retained with a half-time of 0.12 d, 11% with 0.8 d and 5% with 12 d. The half-times of
the two longer retention terms were the same within the experimental errors as those observed
after injection. The highest concentrations of tellurium were observed in the kidneys, blood,
liver, spleen, femur and lung. Tellurium in blood was almost entirely bound to the protein
content of the red blood cells. The tissues could be divided into three classes according to theretention half-time: lung, blood, liver and heart with a half-time of approximately 10 d;muscle, spleen, and kidney with a half-time of approximately 20 d; and femur (skeleton) witha half-time that was much longer than the duration of the experiment (200 d) and could
therefore not be determined with much confidence. About 27% of the injected tellurium was
excreted in urine during the first 24 h, and 6% was excreted in faeces. Less than 0.25% of theadministered dose was eliminated in the breath in the first 24 h, despite a strong garlic odour.
(155) A series of studies on rats were conducted in the years between 1960 and 1970 in theformer USSR and Czechoslovakia. Their findings are summarized by a document of the
Health Council of Netherlands (2002). After intravenous injection tellurium was foundmainly in the liver (10 to 20%), muscle (around 10%) and skeleton (8 to 24%), and to a lesser
extent in the kidneys (2.5-7%). Deposition patterns varied with time from administration,with skeleton being the organ with the greatest retention time. Urinary excretion amounted to
14% of the iv dose on day 1 and 33% in the first week.
(156) Agnew and Cheng (1971) investigated protein binding of tellurium in maternal andfetal tissues after intravenous injection of tellurous acid (H2TeO3) labelled with 127mTe into
pregnant rats. Activity in whole blood was predominantly in the red cells at all times studied.
The fraction in red cells increased from 65% after 15 minutes to about 95% after one week.
By far the bulk of the activity in plasma was in a bound form. After 1 hr of circulation, lessthan 5% of the 127mTe was in unbound form, and only about 0.5% was unbound after one
week.
(157) Mullen and Stanley (1974) studied absorption, distribution and milk secretion ofradiotellurium in dairy cows and calves. The transfer of tellurium to milk was very low (about
0.25% of the orally administered activity in 13 days). Retained tellurium was found mainly inthe liver, bone, and organs of the digestive/ruminal tract. Again, tellurium concentration in53

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2132
2133
2134
2135
2136
2137
2138
2139
2140
2141
2142
2143
2144
2145
2146
2147
2148
2149
2150
2151
2152
2153
2154
2155
2156
2157
2158
2159
2160
2161
2162
2163
2164
2165
2166
2167
2168
2169
2170
2171
2172
2173
2174

the thyroid was significant (about the same order as in the liver), but due to the tiny mass of
this organ the total amount retained was negligible.
(158) Valkonen and Savolainen (1985) administered tellurium in the form of TeCl4 in thedrinking water of rats for up to 35 days. The tellurium concentration in liver remained
constant with time but increased steadily in blood, kidney and brain. The concentration ratio
liver : kidney was 4.1 after 7 days of administration and 2.1 after 35 days. The ratio liver :brain decreased from 8.1 to 1.8 in the same interval.
(159) Morgan et al. (1997) administered cadmium telluride intra-tracheally to rats. Afterabsorption of tellurium into the systemic circulation, significant concentrations were found in
the spleen (maximum, 82.8±10.2 µg⋅g-1 tissue), kidney (maximum, 8.1±1.3 µg⋅g-1 tissue),liver (maximum, 8.8±0.6 µg⋅g-1 tissue), femur (maximum 3.5±0.5 µg⋅g-1 tissue) and blood(maximum, 5.3±0.2 µg⋅g-1 tissue). The maximum concentration was reached at day 14 afteradministration in all tissues except liver, where the maximum was reached at day 7.
4.2.3.2. Biokinetic model for systemic tellurium(160) ICRP Publication 67 (1993) introduced a simple systemic model for tellurium basedon findings in animal studies. That model assumed that 50% of tellurium entering blood goes
directly to excretion with a half-time of 0.8 days; 25% is translocated to the skeleton, fromwhich it is removed to excretion pathways with a half-time of 10,000 days; and the rest isdivided between the kidneys (2.3%), thyroid (0.2%), and remaining tissues (22.5%), fromwhich it is removed to excretion pathways with a biological half-time of 20 days. A urinary tofaecal excretion ratio of 4:1 was assumed for systemic tellurium.
(161) In this report the generic model structure for bone-surface-seeking radionuclides isapplied to tellurium, with the introduction of the thyroid as a separate compartment primarily
to enable the application of the model to tellurium radionuclides produced as progeny ofradioiodine. Transfer coefficients of the model are listed in Table 4-6. These coefficients are
based predominantly on human data with regard to whole body retention and urinary
excretion and on animal data, mainly from studies with swine and guinea pigs, with regard to
the organ distribution.
(162) The compartment called Blood in the generic model structure is divided into two
compartments: Blood 1, representing blood plasma, and Blood 2, representing red blood cells.
It is assumed that tellurium leaves Blood 1 at the rate 1.16 d-1 (half-time of ~0.6 d) with 65%
moving to the urinary bladder contents, 10.5% to Liver, 8.75% to Blood 2, 5.25% to Bone
Surfaces (in the ratio 2:1 between trabecular and cortical), 3.5 % to Kidneys, 0.35% toThyroid and the remaining 19 % to Soft-Tissue compartment ST. The following removal
half-times are assigned: 10 d from Blood 2, Kidney, Thyroid and ST to Blood 1; 10 d from
Liver to the small intestine contents (representing removal from the liver in bile); and 50 dfrom cortical or trabecular bone surface, with 98% returning to Blood 1 and 2% moving to thecorresponding bone volume compartment. The transfer coefficients describing the rates of
movement from the bone volume compartments to Blood 1 are the generic turnover rates forcortical and trabecular bone.

54

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

2175
2176
2177
2178

Figure 4-1. The systemic model for tellurium.
Table 4-7. Transfer coefficients for systemic tellurium
From
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 2Liver
Thyroid
KidneysST
Cortical bone surface
Trabecular bone surface
Cortical bone surface
Trabecular bone surface
Cortical bone volume
Trabecular bone volume

2179
2180
2181
2182
2183
2184
2185
2186
2187

To
Urinary bladder contents
Kidneys
Liver
Blood 2
ST
Cortical bone surface
Trabecular bone surface
Thyroid
Blood 1
Small intestine contents
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Cortical bone volume
Trabecular bone volume
Blood 1
Blood 1

Transfer coefficient (d-1)
0.751
0.04040.12130.10110.07680.02020.04040.00400.06930.06930.06930.06930.06930.01160.01160.0006931
0.0006931
0.0000821
0.000493(163) No explicit exhalation pathway was introduced in the model as the available studies
indicate that, in spite of the persistent garlic odour experienced after tellurium incorporation,
the amount exhaled is negligible.
(164) The transfer coefficients listed in Table 4-7 yield the following predictions, which
are reasonably consistent with the biokinetic database for tellurium summarized above.
Urinary excretion of systemic tellurium is rapid and amounts to 45% in the first 24 h, 64%
after 3 days, 71% after 10 d and 81% after 50 d. These values are in agreement with theurinary excretion observed by Kron et al. (1991) after oral administration of tellurium, taking
55

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2188
2189
2190
2191
2192
2193
2194
2195
2196

into account the absorbed fraction of 0.3. Faecal excretion of intravenous tellurium amounts
to 0.54% after 3 days, 4.4% after 10 days and 12.3% after 50 days. Whole body retention is to55% after one day, 23.8% after 10 d and 2.75% after 100 d, in satisfactory agreement with thedata presented by Fehér and Andrási (1977) and with the curve predicted by them, as shownin Figure 4-2. At five days after intravenous injection, 8.2% of the injected amount iscontained in the liver, 5.2% in the skeleton, 2.7% in the kidneys and 0.27% in the thyroid. At
100 days the retained fractions are 2.4%, 0.1%, 0.03% and 0.003% for skeleton, liver, kidneys
and thyroid respectively.

WB retention (%)

100

10Equation from Feher and Andrasi (1977)
Current model

0.1
2197
2198
2199
2200
2201
2202
2203
2204
2205
2206
2207
2208
2209
2210
2211

1

10

100

Time after incorporation (d)Figure 4-2. Whole body retention for tellurium.
Data from Fehér and Andrási (1977). Grey symbols: retention measured in volunteers after administration of
TeO2-131I suspension. Black symbols: retention measured after accidental contamination by workers. Solid line:
equation suggested by Fehér and Andrási (1977) on the basis of their data. Dashed line: prediction of the OIR
model. For the sake of comparison the workers' values were normalized to the curve prediction for the firstavailable measurement time, as extrapolated from the original graph.

4.2.3.3. Treatment of radioactive progeny(165) Chain members addressed in the derivation of dose coefficients for tellurium
isotopes are isotopes of tellurium, antimony, iodine, or xenon. Isotopes of tellurium,
antimony, or iodine produced in systemic compartments are assumed to follow thecharacteristic models for these elements (i.e. the models applied in this report to theseelements as parent radionuclides) from their time of production, insofar as application of this56

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2212
2213
2214
2215
2216
2217
2218
2219
2220
2221
2222
2223
2224
2225
2226
2227
2228
2229
2230
2231
2232
2233
2234
2235
2236
2237
2238
2239
2240
2241
2242
2243
2244
2245
2246
2247
2248
2249
2250
2251
2252
2253
2254
2255
2256
2257
2258
2259

assumption is straightforward. In some cases, the site of production of antimony or iodine due
to decay of a tellurium isotope may not be clearly identifiable with a specific compartment in
its characteristic biokinetic model due to differences in model structures for the different
elements. In such cases a transfer rate from the site of production of the radionuclide to thecentral blood compartment in the radionuclide’s characteristic model has been assigned as
described below. After reaching its central blood compartment, the radionuclide is assumed tobehave as described by its characteristic model.
(166) Antimony atoms produced in soft-tissue compartments in the tellurium model thatare ambiguous with regard to the characteristic model for antimony (specifically, Liver,
Thyroid, and Other) are assumed to be transferred to the central blood compartment of thatmodel (blood plasma) at the rate 0.693 d-1 (half-time of 1 d). This is the highest rate ofremoval from all soft tissue compartments in the characteristic model for antimony.
Antimony produced in the compartment of the tellurium model called Blood 2, representing
relatively long retention in blood, is assumed to transfer to plasma in the antimony model at
the rate 1000 d-1 (a default rate representing rapid transfer between compartments). For
modelling convenience, antimony produced in the central blood compartment of the tellurium
model (Blood 1) is assigned to plasma in the antimony model.
(167) Iodine atoms are produced at the following sites in the tellurium model that are notclearly identifiable with specific compartments of the characteristic model for iodine:compartments of blood, bone, liver, kidneys, thyroid, and other soft tissues (Other). The
following rates of transfer from these sites to the blood iodide pool of the characteristic model
for iodine are assigned: from compartments of liver or kidneys, 100 d-1 (the rate of loss fromthe liver iodide and kidney iodide compartments in the characteristic model for iodine); fromcompartments of blood (other than the central blood compartment), 1000 d-1; fromcompartments of other soft tissues or bone surface, 330 d-1 (the highest transfer coefficient toblood in the characteristic model for iodine); from thyroid, 36 d-1 (the transfer coefficientfrom the thyroid iodide pool to the blood iodide pool in the characteristic model for iodine);and from trabecular and cortical bone volume compartments, the reference rates of trabecularand cortical bone turnover. For modelling convenience, iodine produced in the central blood
pool of the tellurium model is assigned to the blood iodide pool in the characteristic model
for iodine.
(168) A generic biokinetic model is applied in this report to xenon isotopes produced bydecay of a radionuclide in systemic compartments. Xenon produced in bone is assumed totransfer to blood at the rate 100 d-1 if produced in bone surface and 0.36 d-1 if produced inbone volume. These rates are taken from the model for radon introduced in ICRP Publication
67 (1993) and applied in this report to radon produced in bone surface and non-exchangeablebone volume, respectively, by decay of a radium isotope. Xenon produced in a soft-tissuecompartment is assumed to transfer to blood with a half-time of 20 min. Xenon produced in
the central blood compartment in the model for tellurium, antimony, or iodine is assigned tothe blood compartment of the xenon model. Xenon produced in any other blood compartmentin the tellurium, antimony, or iodine model is assumed to be transferred to blood in the xenon
model at the rate 1000 d-1. Xenon entering the blood compartment of the xenon model orproduced in that compartment is assumed to be removed from the body (exhaled) at the rate
1000 d-1. Partial recycling of xenon to tissues via arterial blood is not depicted explicitly inthis model for xenon as a daughter radionuclide but is considered in the assignment of thehalf-times in tissues. The model is intended to yield a conservative average residence time ofxenon atoms in the body after their production in systemic pools.

57

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2260
2261
2262
2263
2264
2265
2266

4.3. Individual monitoring
129

Te(169) 129Te is a γ emitter. Monitoring of 129Te may be accomplished through Whole Body
Counting. Urine bioassay may also be used. Because of the short half-life measurements
should be done soon after exposure, maximum of 3h after exposure.
IsotopeMonitoring
Technique

129

Urine Bioassay

129

Whole
Counting

Te
Te

2267
2268
2269
2270
2271

Body γ-ray spectrometry

Achievabledetection limit

1070 Bq

Te(170) 131Te is a γ emitter. Monitoring of 131Te may be accomplished through Whole Body
Counting, immediately after exposure (up to three hours).
IsotopeMonitoring
Technique

129

Whole
Counting

MethodMeasurementof Typical
Detection
Limit
Body γ-ray spectrometry 428 Bq

Achievabledetection limit

131m

Te
(171) 131mTe is a γ emitter. Monitoring of 131mTe may be accomplished through Whole
Body Counting. Urine bioassays may also be used. Measurements should be done in a shortperiod after exposure.
IsotopeMonitoring
Technique

129

Urine Bioassay

129

Whole
Counting

Te
Te

2278
2279
2280
2281
2282

of Typical
DetectionLimit
γ-ray spectrometry 331 Bq/L

131

Te

2272
2273
2274
2275
2276
2277

MethodMeasurement

MethodMeasurementof Typical
DetectionLimit
γ-ray spectrometry 1.4 Bq/L

Body γ-ray spectrometry

Achievabledetection limit

395 Bq132

Te(172) 132Te is a γ emitter. Monitoring of 131mTe may be done through Whole Body
Counting. Urine bioassays are also used.
IsotopeMonitoring
Technique132

Urine Bioassay

132

Whole
Counting

Te
Te

MethodMeasurementof Typical
DetectionLimit
γ-ray spectrometry 0.5 Bq/L

Body γ-ray spectrometry

58

100 BqAchievabledetection limit

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
2283
2284
2285
2286
2287
2288

2289
2290
2291
2292
2293
2294
2295
2296
2297
2298
2299
2300
2301
2302
2303
2304
2305
2306
2307
2308
2309
2310
2311
2312
2313
2314
2315
2316
2317
2318
2319
2320
2321
2322
2323
2324
2325

133m

Te
(173) 133mTe is a γ emitter. Monitoring of 133mTe may be accomplished through Whole
Body Counting. Urine bioassays may also be used. Measurements should be done
immediately after exposure (up to three hours).
IsotopeMonitoring
Technique

MethodMeasurement

133m

Te

Urine Bioassay

133m

Te

Whole
Countingof Typical
DetectionLimit
γ-ray spectrometry 114 Bq/L

Body γ-ray spectrometry

Achievabledetection limit

95 Bq

References
Agnew, W.F., Cheng, J.T., 1971. Protein binding of tellurium-127m by maternal and fetal tissues of
the rat. Toxicol. Appl. Pharmacol. 20, 346-356.
Balonov, M., Kaidanovsky, G., Zvonova, I., Kovtun, A., Bouville, A., Luckyanov, N., Voillequé, P.,
2003. Contributions of short-lived radioiodines to thyroid doses received by evacuees fromthe Chernobyl area estimated using early in vivo activity measurements. Radiat. Prot.
Dosim. 105 (1–5) 593–599.
Barnes, D.W.H., Cook, G.B., Harrison, G.E., Loutit, J.F., Raymond, W.H.A., 1955. The metabolismof 132tellurium-iodine mixture in mammals. J. Nucl. Energy 1, 218-230.
Blackadder, E.S., Manderson, W.G., 1975. Occupational absorption of tellurium: a report of twocases. Brit. J. Ind. Med. 32, 59–61.
Casey, H.W., Case, A.C., McClellan, R.O., Bustad, L.K., 1963. Metabolism of Te132-I132 in lactating
sheep. Health Phys. 9, 1223-1226.
Chertok, R.J., Kake, S., 1970. Availability in the dog of radionuclides in nuclear debris from thePlowshare excavation cabriolet. Health Phys. 19, 405-409.
DeMeio, R.H., Henriques, F.C., 1947. Excretion and distribution in tissues studied with a radioactive
isotope. J. Biol. Chem. 169, 609-617.
Dobryakova, G.V., 1970. Dynamics of the removal of Te-127 and Ru-106 from rat lungs. In:
Moskalev, Yu. I., Editor. Radioaktiv. Izotopy Vnesh. Srede Organizme. pp. 57-63. Moscow:
Atomizdat.
Fehér, I. (1976) Investigations of the Internal Radiation Burdens. PhD Thesis (in Hungarian).
Fehér, I. and Andrási, A. (1977) Study on internal contamination due to tellurium isotope mixture.
Proc. 4th IRPA congress Vol 2. pp. 421-424. International Radiation Protection Association.
Geary, D. L., Myers, R. C., Nachreiner, D. J. and Carpenter, C. P. (1978). Tellurium and tellurium
dioxide: single endotracheal injection to rats. Am. Ind. Hyg. Assoc. J. 39, 100-109.
Health Council of the Netherlands (2002). Committee on Updating of Occupational Exposure Limits.
Tellurium and tellurium compounds (excluding TeF6); Health-based Reassessment of
Administrative Occupational Exposure Limits. The Hague: Health Council of theNetherlands, 2000/15OSH/055.
Hollins, J.G. (1969) The metabolism of tellurium in rats. Health Phys. 17, 497-505.
ICRP (1979) International Commission on Radiological Protection. Limits on Intakes ofRadionuclides for Workers. ICRP Publication 30, Pt.1. ICRP 2, (3/4), 85-87.
ICRP (1993) International Commission on Radiological Protection. Age-dependent Doses toMembers of the Public from Intake of Radionuclides. Pt.2. ICRP Publication 67. Ann.
ICRP. 23, (3/4), 61-67.

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2349

Kron, T., Hansen, Ch. and Werner, E. (1991) Renal excretion of tellurium after peroral
administration of tellurium in different forms to healthy humans. J. Trace Elem.
Electrolytes Health. Dis. 5, 239-244
Morgan, D.L., Shines, C.J., Jeter, S.P., Blazka, M.E., Elwell, M.R., Wilson, R.E., Ward, S.M., Price,
H.C., Moskowitz, P.D., 1997. Comparative pulmonary absorption, distribution, and toxicity
of copper gallium diselenide, copper indium diselenide, and cadmium telluride in SpragueDawley rats. Toxicology & Applied Pharmacology, 147, 399–410.
Mullen, A.A., Stanley, R.E., 1974. Absorption, distribution and milk secretion of radionuclides by
dairy cows. III. Radiotellurium. Health Phys. 27, 279-284.
Nason, A.P., Schroeder, H.A., 1967. Abnormal trace elements in man: tellurium - Erratum. J. Chron.
Dis. 20, 671.
Schroeder, H.A., Buckman, J., Balassa, J.J., 1967. Abnormal trace elements in man: tellurium. J.
Chron. Dis. 20, 147-161.
Taylor, A., 1996. Biochemistry of tellurium. Biol. Trace Elem. Res. 55(3), 231-239.
Valkonen ,S., Savolainen, H., 1985. Tellurium burden and neurochemical effects in moderate peroral
exposure. Bull. Environ. Contam. Toxicol. 34, 170-174.
van Montfort, PFE, Agterdenbos, J., Jütte, B.A.H.G., 1979. Determination of antimony and tellurium
in human blood by microwave induced emission spectrometry. Anal. Chem. 51, 1553-1557.
Venugopal, B., Luckey, T.D., 1978. Metal Toxicity ion Mammals. Vol. 2. Plenum Press, New York.
Wright, P.L., Bell, M.C., 1966. Comparative metabolism of selenium and tellurium in sheep andswine. Am. J. Physiol. 20, 6-10.

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5. IODINE (Z = 53)
5.1.

Chemical Forms in the Workplace(174) Iodine is a volatile halogen existing mainly in oxidation states –I, 0 and V. The mostcommon chemical forms of iodine in solution are the iodide (I-) and the iodate (IO3-). Iodine
may be encountered in industry in a variety of chemical and physical forms, including
vapours and gases, organic compounds such as methyl and ethyl iodide, and particulate forms
including metal-iodide (NaI, AgI).
(175) 131I, 129I and 132I (from 132Te) are the three main iodine fission products that are
released from reactor accidents and that are present in fragments of irradiated fuels. 123I and125
I are used in medicine as tracers for imaging and evaluating the function of the thyroid, and131
I is used in medicine for the treatment of thyroid cancer.
Table 5-1. Isotopes of iodine addressed in this report
Isotope
I-118
I-119
I-120
I-120m
I-121
I-123
I-124
I-125a
I-126
I-128
I-129a
I-130
I-131a
I-132
I-132m
I-133
I-134
I-135

2367
2368
2369
2370
2371
2372
2373
2374
2375
2376
2377
2378
2379
2380

a

Physical half-life
13.7 m19.1 m81.6 m53 m
2.12 h
13.27 h4.176 d59.40 d12.93 d24.99 m
1.57E+7 y12.36 h8.021 d2.295 h1.387 h20.8 h52.5 m
6.57 hDecay mode
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+EC
EC, B+EC
EC, B+, BB-, EC, B+
BBBBIT, BBBB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

5.2.

Routes of Intake

5.2.1. Inhalation
Absorption Types and Parameter Values(176) Detailed information on the behaviour of inhaled gases and vapours of iodine isavailable from studies in human volunteers. Hence, although information is also available
from animal experiments, it is not reviewed here. Some information is available on inhaledparticulate forms of iodine: as iodide from animal experiments; and associated with irradiatedfuel fragments from human exposures.
(177) Absorption parameter values and Types, and associated fA values for gas and vapour
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2428

forms of iodine are given in Table 5-2 and for particulate forms in Table 5-3. Exposures toboth gas/vapour forms and particulate forms of iodine are common, and it is therefore
proposed here that in the absence of information 50% particulate; 50% gas/vapour should beassumed (ICRP, 2002a).
(a)

Gases and vapours

Elemental iodine(178) Iodine in thyroid measurements were made up to about 4 months after intake on five
workers who accidentally inhaled 125I vapours released from an open beaker (Bordell et al.,1972). The thyroid activity fell by about 30% between the first two measurements (at 0.5 and
4 days after the intake), suggesting that most of the absorption to blood had occurred by thetime of the first measurement, and indicating Type F behaviour.
(179) Detailed studies have been conducted in human volunteers of the deposition andsubsequent biokinetics of iodine inhaled as vapour labelled with 132I (Morgan et al., 1968a;
Black and Hounam, 1968). The results confirmed the rapid absorption seen previously inanimal experiments. In the experiments conducted by Morgan et al. the iodine was inhaledthrough a mouthpiece. Respiratory tract deposition was almost complete, and the authors
noted that this must be due to the high chemical reactivity of iodine, because it is only
sparingly soluble in water. Measurements with collimated detectors showed high depositionin the oral pharynx, and transfer downwards, presumably to the stomach. From these andmeasurements of systemic activity it was inferred that much of the activity was swallowed
and subsequently absorbed from the alimentary tract. The authors concluded that the main siteof deposition was the oral pharynx, and while penetration to the trachea and bronchi could not
be excluded, it was unlikely that iodine vapour reaches the alveoli. In the experiments
conducted by Black and Hounam the iodine was drawn in through the nose and out throughthe mouth. Using a similar technique, Pattle (1961) reported negligible penetration of the noseand mouth by iodine vapour. However, Black and Hounam found that deposition was notcomplete (typically ~70%) and estimated that in normal breathing rather less than 50% of
iodine vapour would be deposited in the "nasopharyngeal region" and the rest in the
tracheobronchial region. Measurements of retention in different parts of the nasal passage
were made with collimated detectors from 5 to 100 minutes after deposition. These showedthat there was some deposition in the nasal vestibule (ET1), but the fraction deposited there
was not estimated. They estimated a clearance half-time from the nasopharynx of about 30
minutes, but this would not have included clearance during the first few minutes.
(180) Analyses of the results of these human volunteer experiments were carried out by the
Task Group to estimate the rate of absorption of iodine from respiratory tract to blood (sr)following its inhalation in elemental form. A compartment model was set up using the
updated HRTM and the systemic model for iodine described below, and applied to estimate
values of fractional regional deposition and sr using the reported measurements of 132I in the
thyroid and urine. Some parameter values in the systemic model were normalised to theindividual subject using reported measurements of 132I in the thyroid and urine following
ingestion of 132I-labelled sodium iodide by the same subject. From the reported observations(see above) and for simplicity, it was assumed that deposition occurred only in ET2 and BB. It
was found that the results were insensitive to the ratio of deposition between these regions
and the assumption was made of 50% deposition in ET2 and 50% in BB. On that basis, therate of absorption of iodine from respiratory tract to blood (sr) was estimated to beapproximately 100 d–1. As described below, based on this assessment, and the results of62

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2476

studies in which iodine was deposited in the respiratory tract as sodium iodide and in acaesium chloride vector, a value of sr of 100 d–1 is applied here to Type F forms of iodine.
Hence for elemental iodine it is assumed here that there is 100% deposition in the respiratory
tract but in the upper airways (50% ET2 and 50% BB), with Type F absorption.
Methyl iodide (CH3I)(181) Detailed studies have been conducted in human volunteers of the deposition andsubsequent biokinetics of iodine inhaled as CH3I (Morgan et al., 1967a,b; Morgan andMorgan, 1967). The amount retained varied from 50 to 90% (average 70%), increasing withdecreasing number of breaths per minute. It was inferred that most of it deposited in thealveoli. Absorption to blood of the deposited activity was very rapid (estimated half-time
about 5 seconds). Subsequent biokinetics were very similar to those of injected iodide,suggesting that the CH3I is rapidly metabolised. For methyl iodide it is therefore assumed
here that there is 70% deposition in the respiratory tract (with default regional distribution,
Table 5-2) and Type V absorption.
Ethyl iodide (C2H5I)(182) The retention of 132I-labelled ethyl iodide (C2H5I) inhaled by human volunteers wasin the range 44 to 62%, slightly lower than the same group of subjects exposed to methyl
iodide (53 to 81%) (Morgan et al, 1968b). Urinary excretion of 132I also occurred at a slower
rate than that following inhalation of 132I-labelled methyl iodide. For ethyl iodide it istherefore assumed here that there is 60% deposition in the respiratory tract (with default
regional distribution, Table 5-2) and Type V absorption.
(b)

Particulate aerosols

Sodium iodide (NaI)(183) Iodine inhaled as sodium iodide is rapidly absorbed into blood. Thiéblemont et al.
(1965a,b) studied excretion and thyroid uptake of 131I following inhalation of 131I-labelled NaI
by rhesus monkeys, and noted that excretion was similar to that for intravenously injected
131
I. Perrault et al. (1967) investigated the absorption from the respiratory tract of 131I
following inhalation of 131I-labelled NaI by rhesus monkeys. At 13 minutes after the end of a
30-minute exposure, 82% of activity had been absorbed from the respiratory tract to blood. A
compartment model fit by the authors to measurements of 131I in lung and blood gave a halftime for absorption between 2.5 and 10 minutes, i.e. a rate of the order of 100 d–1. Dawson etal. (1985) measured absorption of 131I in isolated perfused rabbit lung exposed to an aerosol
containing 125I-labelled NaI. They calculated a half-time for absorption of about 10 minutes,
corresponding to a rate of ~100 d–1. Although specific parameter values for sodium iodide
based on in vivo data are available, they are not adopted here. Instead, sodium iodide is
assigned to Type F. However, the data are used as the basis for the default rapid dissolution
rate for iodine. Hence specific parameter values for sodium iodide would be the same as
default Type F iodine parameter values.
Caesium chloride vector(184) Thomas et al. (1970) followed the biokinetics of 131I for 70 days after inhalation of131
I associated with caesium chloride vector aerosols by rats. Immediately after the 10-minuteexposure the lung contained only about 1% of the initial body content. By 24 hours, there
were high concentrations in thyroid and pelt. Whole-body retention to 70 days was similar to63

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that in rats following intravenous injection of 131I. Thus absorption from lungs to blood was
rapid, of the order of 100 d–1. The biokinetics of 131I were followed for 30 days after
inhalation of 131I associated with caesium chloride vector aerosols by dogs (McClellan and
Rupprecht, 1968). It was noted that the maximum thyroid uptake (as a fraction of initial bodycontent) and the time after intake at which the maximum thyroid uptake was reached werevery similar for inhaled, ingested, or intravenously injected 131I, which demonstrated thesoluble nature of iodide in body fluids. Although specific parameter values for iodine in acaesium chloride vector based on in vivo data are available, they are not adopted here.
Instead, it is assigned to Type F. However, the data are used as the basis for the default rapid
dissolution rate for iodine. Hence specific parameter values would be the same as default
Type F iodine parameter values.
Silver iodide (AgI)(185) Following inhalation of 131I-labelled silver iodide by mice and sheep (Bair, 1961;
Willard and Bair, 1961), the 131I was rapidly absorbed from the lungs, even though silver
iodide was studied because it is one of the most insoluble iodine compounds in water. Lung
retention of 110mAg following inhalation of 110mAg-labelled silver iodide by dogs and rats
(Morrow et al., 1968) was consistent with assignment to Type M (see silver section).
However, Morrow et al. noted that during aerosolisation some conversion to silver oxide
probably occurs. Hence it appears that the rapid absorption of 131I observed by Bair et al. is
probably not inconsistent with the slow absorption of silver reported by Morrow et al., andiodine inhaled as silver iodide is assigned here to default Type F.
Irradiated fuel fragments(186) Mirell and Blahd (1989) made whole-body measurements of activity on seven people
from about two weeks to several months after exposure to the initial Chernobyl reactor
accident plume in Kiev, Ukraine. Biological retention half-times were similar for different
radionuclides (23 days for 131I) and different from those expected for systemic retention,
indicating that they were trapped in particles and metabolically inert, thus indicating Type M
rather than Type F behaviour.
(187) In view of the limited information available, these data are judged to be an
insufficient basis to provide specific absorption parameter values. Considerable variability
has been observed in the behaviour of caesium associated with irradiated fuel fragments (seecaesium section), for which much more information is available. Since this is also likely tobe the case for iodine, this form is not assigned specifically to a default Type here.
Default rapid dissolution rate for iodine(188) Studies with elemental iodine, sodium iodide, and iodine in a caesium chloride
vector outlined above give values of sr of about 100 d–1, which is applied here to all Type F
forms of iodine.
Extent of binding of iodine to the respiratory tract(189) Evidence from the various experimental studies outlined above suggests that there is
probably little binding of iodine. It is therefore assumed that for iodine the bound state can beneglected, i.e. fb = 0.0.

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Table 5-2. Deposition and absorption for gas and vapour forms of iodinea

Chemical
form/origin
Elemental iodine, I2
Methyl iodide, CH3I
Ethyl iodide, C2H5I
Unspecifieda
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2532
2533
2534
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2538
2539
2540
2541

a

b

c

d

Fraction deposited (%)b
Total ET1
ET2
100
0
50
c
70
0
14
c
60
0
12
100
0
50

BB
50
7
6
50

bb
0
14
12
0

Absorption
Type fA
F
1.0
V
(d)
V
(d)
F
1.0

AI
0
35
30
0

For iodine in unspecified gas or vapour form, the behaviour assumed is the same as that for elemental iodine:
100% deposition (50% ET2 and 50% BB) with Type F absorption.
Fraction deposited refers to how much of the material in the inhaled air remains in the body after exhalation.
Almost all inhaled gas molecules contact airway surfaces, but usually return to the air unless they dissolve in,or react with, the surface lining.
Since instantaneous absorption to blood (Type V) is assumed, calculations can be performed assuming direct
injection into blood, and the regional deposition does not need to be considered. Nevertheless, forcompleteness, the deposits in each region are assumed to be distributed in the same proportions as in thedefault distribution for gases and vapours: 20% ET2, 10% BB, 20% bb and 50% AI.
Not applicable for absorption Type V, because all activity deposited in the respiratory tract is instantaneously
absorbed.

Table 5-3. Absorption parameter values for inhaled particulate forms of iodine and for ingested
iodineAbsorption
parameter Absorption fromvaluesathealimentaryfrsr (d–1) ss (d–1)
tract, fA

Inhaled particulate materials
Default parameter valuesb,cAbsorption
Assigned forms
TypeF
Sodium iodide; caesium chloride 1
vector,silveriodide,allunspecified formsd
M
—
0.2
S
—
0.01
Ingested materials
All unspecified forms
2542
2543
2544
2545
2546
2547
2548
2549
2550
2551
2552
2553
2554
2555

a

b

c

d

100

–

1

3
3

0.005
1x10-4

0.2
0.01

1

It is assumed that for iodine the bound state can be neglected i.e. fb = 0. The value of sr for Type F forms of
iodine (100 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
Materials (e.g. sodium iodide) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see text).
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of iodine (1.0).
Default Type F is recommended for use in the absence of specific information, i.e. if the form is unknown, or
if the form is known but there is no information available on the absorption of that form from the respiratory
tract.

5.2.2. Ingestion(190) The absorption of iodide from the gastrointestinal tract of humans is virtually

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2600
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2602
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complete with reported values of 0.9 and greater (Riggs, 1952; Willard and Bair, 1961;
Wayne et al, 1964; Underwood, 1971). Keating and Albert (1949) reported a rate ofabsorption of about 5% min-1 in fasted individuals, with complete absorption within 2 hours.
Iodide absorption depends, however, on the redox conditions in the gastrointestinal tract.
Mechanistic studies indicate that some oxidizing agents such as chlorine-based disinfectantsoxidize the basal iodide content of the gastrointestinal tract and decrease its bioavailability(Bercz et al., 1986).
(191) For other chemical forms, absorption is less complete. Results obtained for iodine
administered to humans as thyroxine suggested absorption of 0.80 - 0.85 (Wayne et al.,1964). Similar experiments using 125Iodine incorporated in trypsin and given by direct
introduction into the duodenum to one volunteer showed that significant amount ofradioactivity appeared in blood within 4 minutes and increased to a maximum by 75 minutes.
The total activity absorbed in this experiment was about 11% of the ingested activity (LakeBakaar et al., 1980). By contrast, other studies performed on 9 healthy individuals with [131I]labelled trypsin showed absorption of about 0.78-0.98 with a peak of activity in the plasma 1hour after administration (Bohe et al., 1986). These authors showed that only free 131I isabsorbed into the circulation, demonstrating a deiodinating mechanism in the intestine. Thisvariability in iodine absorption between individuals may be partly explained by genetic
polymorphism (Mithen, 2007).
(192) Studies in animals have shown that in dogs, free iodine and iodate are converted toiodide prior to absorption (Cohn, 1932). High values of absorption (>0.7 – 1) have beenreported for absorption of iodine and iodide in goats and cattle, as summarized by Coughtrey
et al. (1983).
(193) In Publication 30 (ICRP, 1979), an absorption value1 of 1 was recommended for all
chemical forms of I. This value was adopted in Publication 56 (ICRP, 1989) for dietaryintakes. An fA of 1 is used here for all forms.
5.2.3.

Systemic Distribution, Retention and Excretion

5.2.3.1. Summary of the database
Iodine requirements in adult humans(194) Iodine is an essential component of the thyroid hormones thyroxine (T4) andtriiodothyronine (T3), which regulate metabolic processes and are critical to growth anddevelopment (Utiger, 2001; BEST, 2005; Delange and Dunn, 2005). Several tens of
micrograms of inorganic iodide are trapped daily by the adult human thyroid and used forsynthesis of T4 and T3. T4 is produced only in the thyroid and represents >90% of thehormonal iodine secreted by the thyroid. About 20% of the circulating T3 is produced in the
thyroid, and the rest is produced from T4 in extra-thyroidal tissues through a process
involving removal of a single iodine atom from T4. T3 is more active than T4 and exerts mostof the effects of the thyroid hormones in the body (Greenspan, 2004; BEST, 2005; Bianco andLarsen, 2005).
(195) Iodine is largely recycled by the body after use of T4 and T3 by tissues, but the
body’s supply must be supplemented with dietary iodine due to obligatory losses in excreta.
The World Health Organization (WHO) recommends daily intake of 150 μg of iodine byadults and 200 μg during pregnancy and lactation to ensure adequate production of thyroid
hormones and prevention of goiter and hypothyroidism (WHO, 2001; FAO/WHO, 2002).
WHO defines dietary iodine intake of 50-99 µg d-1 (or 50-99 µg L-1 urine, assuming a daily
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2633
2634
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2640
2641
2642
2643
2644
2645
2646
2647
2648
2649
2650
2651

urine volume of 1 L and ignoring losses along other excretion routes) as mild iodine
deficiency, 20-49 µg d-1 as moderate iodine deficiency, and <20 µg d-1 as severe iodide
deficiency. Extensive survey data on dietary and urinary iodine (Parr et al., 1992; O’Hare etal., 1998; Iyengar et al., 2004; WHO, 2004; Delange and Dunn, 2005; Caldwell et al., 2005)
indicate that iodine intake is at or above recommended levels in much of the world but ismildly to severely deficient in many regions. Daily intake of iodine typically is 30-40% lower
in women than in men (Oddie et al., 1970, Fisher et al., 1971; Milakovic et al., 2004, Bilek etal., 2005; Burman, 2006; CDC, 2008). The following reference values for dietary iodine are
selected on the basis of worldwide survey data: 130 µg d-1 for women, 190 µg d-1 for men,and 160 µg d-1 as a gender-averaged value.
(196) The following overview of the systemic biokinetics of iodine in adult humans was
excerpted from a review by Leggett (2010).
Absorption and distribution of inorganic iodide(197) Iodine occurs in foods mainly as inorganic iodide. Other forms of iodine in foods
are reduced to iodide in the alimentary tract before absorption (Cohn, 1932; WHO, 1989).
Absorption is primarily from the small intestine but may occur to some extent from thestomach and other sites along the alimentary tract (Cohn, 1932; Riggs, 1952; Small et al.,1961). Absorption is rapid and nearly complete in most cases. Keating and Albert (1949)
estimated an absorption rate of about 5% min-1 in fasted individuals, with virtually complete
absorption within 2 hours. Absorption was slower when iodide was ingested with food but was
virtually complete after about 3 hours. More than 99% of iodine orally administered as
potassium iodide was absorbed to blood in normal subjects (Oddie et al., 1964; Fisher et al.,1965).
(198) Absorbed iodide is distributed rapidly throughout the extracellular fluids (ECF).
Most of the iodide that leaves blood is recycled to blood within 1-2 h and much of it isrecycled within a few minutes (Riggs, 1952; Wayne et al., 1964; Hays and Solomon, 1965).
(199) The iodide ion is largely excluded from most cells but rapidly traverses the red blood
cell (RBC) membrane. Equilibration between plasma iodide and RBC iodide occurs inminutes. The concentration of iodide in RBC water is about the same as in plasma water,
giving about two-thirds as much iodide in the total RBC as in an equal volume of plasma(Myant et al., 1950; Riggs, 1952).
(200) A substantial portion of iodide entering blood is concentrated in the salivary glands
and stomach wall by active transport. It is subsequently secreted into the alimentary tract
contents in saliva and gastric juice and nearly completely reabsorbed to blood. As a central
estimate the rate of clearance of plasma iodide in saliva plus gastric secretions is about 43
ml/min (range, 36-49 ml/min) (Hays and Solomon, 1965; Harden and Alexander, 1968;
Harden et al., 1969). The concentration of iodine in these secretions is on the order of 30
times its concentration in plasma. There is a delay of about 20 min between uptake of iodineby the salivary glands and stomach wall and appearance in the stomach contents, and a delayof about 30 min between the peak concentration in plasma and the peak concentration in
secretions into the alimentary tract (Riggs, 1952; Hays and Wegner, 1965).
(201) The thyroid and kidneys are in competition for blood iodide and hence for the body’s
supply of iodide due to the rapid recycling of total-body iodide through blood. Normallymore than 90% of the loss of iodine from the body is due to renal clearance of iodide. Little
inorganic iodide is lost in faeces. Sweat does not appear to be an important mode of loss of
iodide except perhaps in hot climates or during intense exercise (Wayne et al., 1964; Smythand Duntas, 2005).
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(202) Iodide in blood plasma is filtered by the kidneys at the glomerular filtration rate.
About 70% of the filtered iodide is reabsorbed to blood, and the rest enters the urinary
bladder contents and is excreted in urine (Bricker and Hlad, 1955; Vadstrup, 1993). Renal
clearance expressed as the volume of plasma iodide or blood iodide cleared per unit time isnearly constant over a wide range of plasma concentrations for a given age and gender. As acentral estimate, renal clearance is about 37 ml plasma/min for euthyroid adult males (Berson
et al., 1952; Wayne et al., 1964; Hays and Solomon, 1965). Renal clearance of iodide
expressed as plasma volumes per unit time appears to be about 25-30% lower on average inwomen than in men, but fractional loss of total-body iodide in urine per unit time is similar
for men and women (Wayne et al., 1964; Oddie et al., 1966).
(203) The concentration of radioiodide in the kidneys may exceed that in most
extrathyroidal tissues for a brief period after acute input into blood. In rats the peakconcentration in the kidneys occurred about 15 min after intravenous injection (Korolev,
1969; Esposito, 1970), at which time the kidneys contained a few percent of the injectedamount (Korolev, 1969). In rats and mice the concentration of radioiodine in the kidneys was
similar to that of the salivary glands during the early hours after intravenous or intraperitoneal
injection (Esposito, 1970; Dadachova et al., 2002). Data on laboratory animals generallyindicate that the concentration of radioiodide in the kidneys declines rapidly and is not muchgreater than that of most other organs by a few hours after administration (Ruegamer, 1953;
Ulmer et al., 1959; Moskalev and Yegorova, 1972). Using imaging data for 124I as a tracer
for 131I in patients with thyroid cancer, Kolbert et al. (2007) estimated that the dose to kidneys
from 131I was on average roughly half of the dose to the salivary glands.
(204) Data on the extent of accumulation of inorganic radioiodide in the liver are variable.
It appears from animal data that the liver typically accumulates a few percent of radioiodide
soon after ingestion or intravenous administration but much less per gram of tissue than thekidneys (Willard and Bair, 1961; Korolev, 1969; Moskalev and Yegorova, 1972; Dadachova
et al., 2002; Zuckier et al., 2004).
Behavior of iodide and organic iodine in the thyroid(205) The basic unit of cellular organization within the thyroid is the follicle, a sphericalstructure typically a few hundredths of a millimeter in diameter. Each follicle is composed ofa single layer of epithelial cells enclosing a lumen filled with a viscous material called
colloid. The colloid consists mainly of thyroglobulin, a protein synthesized by follicular cells
and secreted into the lumen. Thyroglobulin serves as a matrix for production and storage ofT4 and T3 (Kopp, 2005).
(206) Iodide is actively transported from blood plasma into thyroid follicular cells at theplasma membrane. A normal thyroid can concentrate the iodide ion to 20-40 times its
concentration in blood plasma. Some of the trapped iodide leaks back into blood, but most of
it diffuses across the follicular cell and enters the follicular lumen where it is converted toorganic iodine.
(207) Berson and Yalow (1955) studied the kinetics of trapping and binding of
intravenously injected 131I by the thyroid in 24 hyperthyroid and 3 euthyroid subjects, firstwith no inhibition of binding and later with administration of a drug that inhibited binding.
They concluded that the rate of binding of trapped iodide is much greater than the rate of
return of trapped iodide to blood. When iodide binding was blocked before administration of
131
I, activity in the thyroid reached a peak at times varying from several minutes to an hour ormore after injection. In about 80% of the cases the rate of loss of trapped 131I from theblocked thyroid was in the range 0.015-0.047 min-1 (22-68 d-1).
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(208) Robertson et al. (1971) estimated the rate of binding of trapped iodide by the thyroid
and the rate of return of trapped iodide to plasma (exit rate) in 15 hyperthyroid and 7
euthyroid subjects by kinetic analysis of time-dependent plasma concentrations and thyroid
accumulation of intravenously injected 131I. The estimated binding rate was significantly
greater in hyperthyroid than in euthyroid subjects, but no significant difference was found in
the exit rate in the two groups. The estimated mean exit rate (+/- standard deviation) for all
22 subjects was 0.025 +/- 0.013 min-1 (36 +/- 19 d-1). Estimates of the binding rate averaged
0.110 +/- 0.042 min-1 (160 +/- 60 d-1) in the hyperthyroid subjects and 0.066 +/- 0.039 min-1(95 +/- 56 d-1) in the euthyroid subjects.
(209) Iodide is transported across the luminal membrane of the follicular cell into thelumen and oxidized at the cell-colloid interface. The neutral iodine atoms formed byoxidation of iodide are bound (organified) within the lumen to specific residues of the aminoacid tyrosine. Some tyrosine residues gain one iodine atom, forming monoiodotyrosine (MIT)and others gain two iodine atoms, forming diiodotyrosine (DIT). T4 is formed within thelumen by the coupling of two DIT molecules and hence has four iodine atoms, and T3 isformed within the lumen by coupling of one MIT molecule to one DIT molecule and hence
has three iodine atoms. The lumen typically contains 10-15 times more T4 than T3.
(210) The thyroid adapts to prolonged reductions or increases in iodine intake by adjusting
its rate of uptake of iodide from blood. Adaptation of thyroidal clearance of iodide to dietaryintake results in an inverse relation between net 24-h thyroidal uptake of ingested radioiodine(U) and average 24-h urinary excretion of stable iodine (E). The uptake rate U also depends
on the mass S of iodine secreted daily by the thyroid. Stanbury et al. (1954) derived theformula U=S/(S+E) or U=[1+(E/S)]-1, based on the assumption that daily accumulation oforganic iodine by the thyroid is in mass balance with daily secretion S of hormonal iodine.
They derived a central estimate for S of 57 μg d-1 from measurements of E and U in a
relatively large study group, primarily young adult females, with generally low rates ofurinary excretion of stable iodine and high incidence of goiter. The formula U=57/(57+E) is
still widely used to estimate thyroidal uptake of radioiodine on the basis of urinary iodide(Ermans, 1993; O’Hare et al., 1998).
(211) Zvonova (1989) compiled regional data on dietary intake or urinary excretion of
stable iodine, thyroidal uptake of radioiodine, and mass of the thyroid in adult humans. Data
were collected for populations in Argentina, West Germany, Russia, Denmark, Scotland,
Hungary, West New Guinea, and seven regions in the U.S. Estimated dietary intake Y of
stable iodine ranged from 5-10 μg d-1 in West New Guinea to 250-700 μg d-1 in some regionsof the U.S. The mean fractional uptake of ingested radioiodine by the thyroid after 24 h (U)was estimated as 0.14-0.15 for populations with intake >400 μg d-1, 0.16-0.27 for intake of
250-330 μg d-1, 0.41-0.45 for intake of 80-85 μg d-1, 0.54-0.59 for intake of 40-54 μg d-1, andabout 0.9 for intake of 5-10 μg d-1. Zvonova derived the relation U = 85/(85+Y) or
U=[1+(Y/85)]-1 based on an assumed balance of daily thyroidal accumulation of organic
iodine and secretion S of hormonal iodine. The value S = 85 μg d-1 was derived by fitting thecollected data for Y and U.
(212) The formulas of Stanbury et al. (1954) and Zvonova (1989) are both broadly
consistent with central estimates of thyroidal uptake of radioiodine in populations withdietary iodine up to a few hundred micrograms per day but substantially underestimate uptake
in populations with iodine-rich diet. The underestimates apparently arise because theassumption of balance of thyroidal uptake and hormonal secretion of iodine is invalid at highlevels of dietary stable iodine. The rate of accumulation of organic iodine by the thyroid andthe rate of loss of iodine from the thyroid both appear to increase at high levels of iodine
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intake, but the mass of iodine secreted as thyroid hormones appears to remain unchanged(Koutras et al., 1964; Fisher et al., 1965; Ohtaki, 1967; Nagataki et al., 1967; Harrison, 1968;
Fisher and Oddie, 1969a).
(213) In adults with iodine sufficient diet the thyroid typically stores 5-15 mg of hormonal
iodine (Riggs, 1952; Fisher and Oddie, 1969b; Hellstern et al., 1978; Handl et al., 1984;
Shapiro et al., 1994; Hays, 2001). Estimates of the rate S of secretion of hormonal iodine by
the thyroid (μg I d-1) in individual euthyroid adult humans range from less than 30 μg d-1 tomore than 150 μg d-1 (Riggs, 1952; Berson and Yalow, 1954; Ingbar and Freinkel, 1955;
Stanbury et al., 1954; Gregerman et al., 1962; Fisher et al., 1965; Fisher and Oddie, 1969a;
Zvonova, 1989). Reference values for adults given in reviews and textbooks generally are in
the range 55-85 μg d-1 (Riggs, 1952; Halnan, 1964; Fisher and Oddie, 1969a; Alexander et al.,1971, DeGroot et al., 1971; Underwood, 1977; Zvonova, 1989). There is a decline of thyroid
hormone secretion with increasing adult age, at least after the fifth or sixth decade(Gregerman et al., 1962; Fisher et al., 1965; Oddie et al., 1965; Herrmann et al., 1981;
Mariotti, 1995; Sawin, 2005). The secretion rate appears to be about one-third lower on
average in women than in men although there is some overlap is measurements for womenand men (Ingbar and Freinkel, 1955; Fisher et al., 1965; Oddie et al., 1965). The following
reference values of S for workers are based on collected data on thyroidal secretion of iodine
as T4 for ages 18-65 y and the assumption that T4 represents 90% of total secretion of
hormonal iodine: 52 μg d-1 for females, 76 μg d-1 for males, and 64 μg d-1 as a genderaveraged value.
(214) Fractional transfer of iodine from thyroid stores to blood per unit time depends on
the size of current stores, the rate of secretion of thyroid hormones, and the extent of leakageof iodide from MIT and DIT deiodinated in follicular cells. For example, assuming firstorder kinetics and negligible leakage of iodide to blood, thyroidal stores of 5 mg and asecretion rate of hormonal iodine of 64 μg d-1 correspond to a half-time of about 54 d; storesof 10 mg and secretion of 76 mg correspond to a half-time of about 91 d; and stores of 15 mg
and a secretion rate of 80 μg d-1 correspond to a half-time of about 130 d. Wellman et al.
(1970) estimated a mean half-time of about 68 d based on data collected from several studies.
In an extensive review of the literature Dunning and Schwartz (1981) determined a range of
21-372 d and a mean of 85 d for adults. Long-term measurements on five workers acutely
exposed to 125I vapor indicated an average biological half-time of about 130 d (Bordell et al,1972). A biological half-time of 90 d is adopted in this report as a reference value for adults.
Behavior of extrathyroidal T4 and T3(215) Upon secretion by the thyroid into blood, T4 and T3 are rapidly and almost
completely bound to plasma proteins. Little if any enters the RBC. As a result of protein
binding, clearance of organic iodine from the circulation is slower than removal of the iodide
ion from the circulation. Reported concentrations of protein-bound iodine in blood plasma of
euthyroid subjects generally are in the range 3-8 μg / 100 ml and cluster about 5-6 μg / 100 ml(Tucker and Keys, 1951; Oppenheimer et al., 1967; Nicoloff and Dowling, 1968; Pittman etal., 1971; Acland, 1971; Nicoloff et al., 1972).
(216) A number of investigators have studied the kinetics of radio-labeled T4 after
intravenous injection into human subjects (Riggs, 1952; Sterling et al., 1954; Ingbar andFreinkel, 1955; Sterling, 1958; Lennon et al., 1961; Gregerman et al., 1962; Cavalieri andSearle, 1966; Oppenheimer et al., 1967; Nicoloff and Dowling, 1968; Wartofsky et al., 1972;
Chopra, 1976; Hays and McGuire, 1980). The removal half-time from blood plasma typicallyincreases from about 1 h at 20-60 min after injection to about 1 wk at equilibrium. Early
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disappearance from plasma may represent mainly distribution throughout the extracellular
fluids plus uptake by hepatocytes. The slower decline at later times may represent uptake bycells and binding to intracellular proteins throughout the body, reduction to inorganic iodide
due to use of the hormones by cells, and biliary secretion followed by faecal excretion of partof the organic iodine entering the liver. External measurements together with liver biopsy
data indicate that the liver accumulates roughly 35% (22-52%) of injected T4 during the first
3-4 hours after administration and contains roughly 25% (14-40%) of extrathyroidal T4 atequilibrium (Cavalieri and Searle, 1966; Oppenheimer et al., 1967; Nicoloff and Dowling,
1968, Hays and McGuire, 1980).
(217) The kinetics of labeled T3 has been difficult to determine with much precision, inlarge part due to interference of iodoproteins generated by metabolism of the injected tracematerial (Nicoloff et al., 1972; Hays and McGuire, 1980). Human studies indicate high initial
uptake of labeled T3 by the liver but a shorter retention time than T4 in the liver (Cavalieri etal., 1970). The liver content at equilibrium has been estimated as 5-21% of the total
extrathyroidal T3 pool (Cavalieri et al., 1970; Hays, 1985).
(218) A portion of T4 or T3 entering the liver is secreted into the small intestine in bile
(Greenspan, 2004). The secreted form is poorly absorbed to blood and is largely excreted in
faeces (Hays, 1985). This accounts for about one-fifth of the loss of organic iodine fromextrathyroidal tissues, and reduction to iodide and return to the blood iodide pool accounts forthe rest (Berson and Yalow, 1954; Ingbar and Freinkel, 1955; Hiss and Dowling, 1962;
Choufoer et al., 1963; Anbar et al., 1965; Hays and Solomon, 1969; Pittman et al., 1971;
Chopra, 1976). Endogenous faecal excretion of organic iodine can become a major source ofloss of iodine during periods of low intake of iodine (Choufoer et al., 1963; Busnardo andCasson, 1965; Kirchgessner et al., 1999).
(219) Animal studies indicate that the concentration of organic iodine in the kidneys is atleast as high as that in the liver. For example, in rats receiving daily injections of 125I over athree-week period, the concentration of labeled T4 in kidneys was similar to that in the liver,about 7 times that in muscle, and more than twice that in heart (Winder and Heninger, 1971).
The concentration of labeled T3 in kidneys was nearly twice that in the liver, 8-9 times that inmuscle, and 4 times that in heart.
(220) Most estimates of the mass of extrathyroidal organic iodine at equilibrium are in therange 500-1000 μg. Most estimates of the biological half-life of T4 in normal subjects are in
the range 5-9 d (Sterling et al., 1954; Ingbar and Freinkel, 1955; Gregerman et al., 1962;
Anbar et al., 1965; Oppenheimer et al., 1967; Nicoloff and Dowling, 1968; Wartofsky et al.,
1972; Chopra, 1976; Hays and McGuire, 1980; ICRP, 1987). The half-life of T3 is about 1 d(Pittman et al., 1971; Nicoloff et al., 1972; Inada et al., 1975; Chopra, 1976; Bianchi et al.,
1978; Hays and McGuire, 1980; BEST, 2005) and that of reverse T3 (rT3) is a few hours(Chopra, 1976). Extrathyroidal conversion of T4 to T3 or rT3 results, in effect, in an extensionof the half-life of T4. Measurements on 73 euthyroid males of ages 18-91 y indicate that therate of T4 production as well as its turnover rate, representing the combined rate of
deiodination and faecal excretion, decrease with age starting some time before age 50 y
(Gregerman et al., 1962). The half-life of labeled T4 was estimated as 6.6 d in young adultmales and 8-9 d after the fifth decade of life (Gregerman et al., 1962). In 165 healthy subjects
in the age range 18-86 y, measured rates of deiodination of T4 were similar in male andfemale subjects in the same age groups (Anbar et al., 1965). The half-time of deiodination of
T4 increased with age from about 8 d in the third decade of life to about 13 in the sixth decade(Anbar et al., 1965).
(221) Nicoloff and Dowling (1968) evaluated the extrathyroidal distribution of 131I-labeled71

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T4 in a group of 13 normal subjects. They interpreted external measurements in terms of afour-compartment model representing blood plasma, extracellular fluid, and hepatic andextrahepatic cellular fluid spaces. Their results indicate that the liver cleared T4 considerably
faster than extrahepatic tissues and contained about 14% of extrathyroidal T4 at equilibrium(Nicoloff and Dowling, 1968). Results of human studies by Oppenheimer et al. (1967)
interpreted in terms of a two-compartment model suggest greater accumulation of T4 in theliver.
(222) In rats receiving daily injections of 125I over a three-week period, the concentrationof labeled T4 in kidneys was similar to that in the liver, about 7 times that in muscle, andmore than twice that in heart (Winder and Heninger, 1971). The concentration of labeled T3
in kidneys was nearly twice that in the liver, 8-9 times that in muscle, and 4 times that inheart.
5.2.3.2.

Biokinetic model for systemic iodine

Previous models(223) A number of physiological systems models have been developed to describe
quantitative aspects of the metabolism of iodine as an essential element in humans (Brownell,
1951; Riggs, 1952; Oddie et al., 1955; Hays and Wegner, 1965; Berman et al., 1968; Nicoloff
and Dowling, 1968; DeGroot et al., 1971; Alexander et al., 1971; McGuire and Hays, 1981;
Bazin et al., 1981; Degon et al., 2008). A three-compartment biokinetic model of iodine
developed by Riggs (1952) for applications in physiological and clinical studies has been usedby the ICRP for many years as the basis of its biokinetic models for occupational orenvironmental intake of radioiodine. The ICRP model with parameter values applied toworkers in recent reports (ICRP, 1994, 1997) is shown in Figure 5-1. The compartments andpaths of transfer represent absorption of dietary iodine to blood as inorganic iodide;competition between thyroidal and renal clearance for circulating inorganic iodide;production, storage, and secretion of hormonal iodine by the thyroid; deiodination of most of
the secreted hormonal iodine and recycling of inorganic iodide; and loss of the remainder ofsecreted hormonal iodine in faeces.
(224) Variations of the Riggs model and some more detailed iodine models beendeveloped for specific applications in radiation protection including: age-specific dosimetryof internally deposited radioiodine for application to environmental exposures (Stather andGreenhalgh, 1983; Johnson, 1987; ICRP, 1989); estimation of doses to patients from medical
applications of radioiodine (MIRD, 1975; Robertson and Gorman, 1976; McGuire and Hays,
1981; Hays, 1985; ICRP, 1987; Johannsson et al., 2003); dose to the embryo/fetus or nursing
infant from intake of radioiodine by the mother (Berkovski, 1999a,b, 2002; ICRP, 2002b);
and reduction of radioiodine dose by administration of potassium iodide (Adams and Bonnell,
1962; Ramsden et al., 1967; Zanzonico and Becker, 2000). The model of Berkovski(1999a,b, 2002) for the pregnant or nursing mother and the model of Johannsson et al. (2003)
designed for applications in nuclear medicine of provide relatively detailed descriptions of theearly biokinetics of inorganic iodide to allow improved dosimetry of short-lived radioiodine.

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Figure 5-1. Biokinetic model for iodine introduced by Riggs (1952) and widely used inradiation protection, with the ICRP’s current parameter values for workers (ICRP,
1994, 1997).
In recent ICRP documents the compartment “All inorganic iodide in body” is called “Blood”, the compartment“Organic iodine in thyroid” is called “Thyroid”, and the compartment “Organic iodine in rest of body” is called“Rest of body”.

Model used in this report(225) The model for systemic iodine used in this report is taken from a paper by Leggett(2010). The model describes the biokinetics of systemic iodine in terms of three subsystems:
circulating (extrathyroidal) inorganic iodide; thyroidal iodine (trapping and organic binding ofiodide, and synthesis, storage, and secretion of thyroid hormones); and extrathyroidal organic
iodine.
(226) The structure of the model including connections with the alimentary tract is shownin Figure 5-2. Baseline transfer coefficients for a male or female worker are listed in Table
5-4.

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Figure 5-2. Structure of the biokinetic model for systemic iodine used in this report.
(227) The modeled behavior of extrathyroidal inorganic iodide is an extension of a modelof Hays and Wegner (1965) based on bioassay and external measurements of 131I in young
adult males during the first 3 h after intravenous injection. The present model adds
compartments representing inorganic iodide in kidneys and liver and adjusts flow rates toaccount for differences in model structure and the size of the blood iodide pool comparedwith the model of Hays and Wegner. The following compartments are used to describe thebehavior of extrathryoidal inorganic iodide: a compartment representing iodide in bloodplasma plus RBC, treated as a well-mixed pool (Blood 1); Salivary glands; Stomach wall;
Liver 1, representing iodide in the liver; Kidneys 1, representing iodide in kidneys; Other 1,
representing rapidly exchangeable iodide in extracellular fluids of extrathyroidal tissues otherthan kidneys and liver; Other 2, representing slowly exchangeable iodide in extrathyroidal
tissues other than kidneys and liver; and a series of compartments representing different
segments of the alimentary tract as represented in the ICRP’s alimentary tract model (ICRP,
2006).
(228) The behavior of iodine in the thyroid is described in terms of two compartments
representing inorganic iodide (Thyroid 1) and organic iodine (Thyroid 2). Thyroid 1 receives
iodide from Blood 1, feeds iodide to Thyroid 2, and leaks some iodide back to Blood 1.
Thyroid 2 converts iodide to organic iodine and transfers organic iodine into the bloodorganic iodine pool (Blood 2). An arrow representing leakage of activity from Thyroid 2 into
Blood 1 is included for application of the model to subjects with unusually high dietaryiodine, but the baseline transfer coefficient from Thyroid 2 to Blood 1 is set to zero.

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(229) The modeled behavior of extrathyroidal organic iodine is an extension of a model ofextrathyroidal T4 kinetics developed by Nicoloff and Dowling (1968) from measurements of131
I-labeled T4 in 13 healthy human subjects (7 women and 6 men). The present model adds acompartment representing organic iodine in the kidneys and assumed to have the same rate ofexchange with blood plasma per gram of tissue as does the liver. The following compartments
are used to describe the behavior of extrathyroidal organic iodine: Blood 2, representing
thyroid hormones bound to plasma proteins; Liver 2, representing organic iodine in liver;
Kidneys 2, representing organic iodine in kidneys; Other 3, representing rapidly exchangeableorganic iodine in extracellular fluids of extrathyroidal tissues other than kidneys and liver;and Other 4, representing slowly exchangeable organic iodine in extrathyroidal tissues otherthan kidneys and liver.
(230) The kidneys and liver are each divided into two compartments to address thedifferent biokinetics of inorganic iodide and organic iodine. The kidneys are treated explicitly
because they accumulate both inorganic iodide and hormonal iodine to a greater extent thanmost extrathyroidal tissues. The liver is treated explicitly mainly because it is an important
repository for hormonal iodine. The iodide content of the liver is addressed for completeness.
(231) Iodine is assumed to be removed from the body only through urinary and faecal
excretion. Iodide moves to Urine after transfer from Blood 1 into Urinary bladder contents.
This represents the net result of glomerular filtration of iodide, reabsorption of much of thefiltered iodide to blood, and transfer of the remainder to the urinary bladder contents followedby excretion in urine. Organic iodine is excreted in faeces after transfer from Liver 2 to Rightcolon, representing the net result of secretion into the small intestine and transfer ofunabsorbed organic iodine to the right colon followed by excretion in faeces.
(232) Assuming that stable iodine intake and excretion are in balance, the transfer
coefficient λ from Blood iodide to Thyroid iodide can be estimated in terms of the dietarystable iodine Y (μg d-1) and the rate S of secretion of stable iodine by the thyroid (μg d-1)
(Leggett, 2010):
λ = 16.34 / [0.98(Y/S) – 0.2] d-1(Eq. 5-1)(233) Thus, λ depends on the ratio Y:S. For example, the ratio Y:S based on reference
values for a male worker is Y: S = 190 μg d-1 : 76 μg d-1 = 2.5. The same ratio is derived
from reference values for a female worker: Y: S = 130 μg d-1 : 52 μg d-1 = 2.5. The resulting
transfer coefficient based on the above formula is 7.26 d-1.

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Table 5-4. Baseline parameter values for the biokinetic model for systemic iodine,applicable to a reference worker.
Pathway

Transfer coefficient
(d-1)
7.26a
11.84
5.16
8.60
600
25
15
50
50
95
36
0.0077
0c
330
35
56
100
100
15
21
1.2
0.62
0.14
3.6
21
0.14
21
21
0.14
0.08

Blood 1 to Thyroid 1
Blood 1 to Urinary bladder contents
Blood 1 to Salivary gland
Blood 1 to Stomach wall
Blood 1 to Other 1
Blood 1 to Kidneys 1
Blood 1 to Liver 1
Salivary gland to Oral cavity
Stomach wall to Stomach contents
Thyroid 1 to Thyroid 2
Thyroid 1 to Blood 1
Thyroid 2 to Blood 2b
Thyroid 2 to Blood 1
Other 1 to Blood 1
Other 1 to Other 2
Other 2 to Other 1
Kidneys 1 to Blood 1
Liver 1 to Blood 1
Blood 2 to Other 3
Other 3 to Blood 2
Other 3 to Other 4
Other 4 to Other 3
Other 4 to Blood 1
Blood 2 to Kidneys 2
Kidneys 2 to Blood 2
Kidneys 2 to Blood 1
Blood 2 to Liver 2
Liver 2 to Blood 2
Liver 2 to Blood 1
Liver 2 to Right colon contents

Depends on the ratio Y/S, where Y (μg d-1) is dietary intake of stable iodine and S (μg d-1) is
the rate of secretion of hormonal stable iodine by the thyroid.
b
For high intake of stable iodine the outflow from Thyroid 2 is split between Blood 2 andBlood 1 as described by Leggett (2010).
c
Non-zero only for high intake of stable iodine (Leggett, 2010).
a

2964
2965
2966
2967
2968
2969
2970
2971
2972
2973

(234) The above formula for the transfer coefficient λ from Blood iodide to Thyroid iodide
is applicable to any combination of Y and S that gives a transfer coefficient of at least 2.5 d-1.
For lower derived values, the transfer coefficient is set at 2.5 d-1. This coefficient together
with baseline values for other coefficients gives a 24-h thyroid content of about 12% of theingested amount. This appears to be a reasonable average value for dietary iodine between
400 and 2000 μg d-1, although considerably variability is seen between individual subjects.
(235) The reader is referred to the paper by Leggett (2010) for a more detailed descriptionof the basis for the model structure and parameter values.

76DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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2975
2976
2977
2978
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2980
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2982
2983
2984
2985
2986
2987
2988
2989
2990
2991
2992
2993
2994
2995
2996
2997
2998
2999
3000
3001
3002
3003
3004
3005
3006
3007
3008
3009
3010
3011
3012
3013
3014
3015
3016
3017
3018
3019
3020

Model predictions(236) In the following, predictions of time-dependent activities in tissues and fluids are
based on the following transfer rates involving stomach and small intestine contents: 20.57 d1
from stomach contents to small intestine contents as a reference value for adult males for
total diet (ICRP, 2006) ; 6 d-1 from small intestine contents to colon contents (ICRP, 2006);
and 594 d-1 from small intestine contents to blood, representing 99% absorption assuming acompeting transfer coefficient of 6 d-1 from small intestine contents to colon contents.
(237) Figures 5-3 and 5-4 show observations (symbols) and model predictions (curves) of
the distribution of radioiodine in the first few hours after intravenous injection into adulthumans. The open circles in these figures represent means for nine healthy young adult males(Hays and Solomon, 1965); variability of measurements was reported as mean coefficients ofvariation, which were approximately 12% and 23% for blood plasma and thyroid,
respectively. The close agreement in Figure 5-3 between predictions and the open circles is to
be expected because the parameter values dominating model predictions in this case werebased in part on these data. The triangles in Figure 5-3 represent median values determinedfrom graphs of data for 5-13 individual euthyroid patients (Berson et al., 1952); individual
measurements varied by less than 15% from the estimated medians. The plus signs in Figures
5-3 and 5-4 were determined from graphs of mean values for 9-10 euthyroid subjects(Alexander et al., 1971); variability of measurements was not reported. The model predictions
shown in Figure 5-3 are for total blood iodide. The comparison with observed values assumes
equilibration between blood plasma and RBC water.
(238) In Figure 5-4 the observations are compared with model-generated curves based on
three different values of the transfer coefficient from blood to thyroid. This transfer
coefficient is derived from Eq. 5-2 and depends on the ratio Y/S, where Y is dietary stableiodine (µg d-1) and S is daily secretion of hormonal iodine by the thyroid (µg d-1). Estimatesof Y and S were not reported for the three study groups addressed in the figure. The grouprepresented by plus signs (subjects of Alexander et al., 1971) was from a region withrelatively low dietary iodine, suggesting a ratio Y/S less than the baseline value 2.5. The
transfer coefficient based on the ratio Y/S = 2 yields reasonable agreement with thyroidal
uptake data for that group as well as data for the healthy young adult male subjects of Hays
and Solomon (1965). Short-term urinary data for the third group, represented by the single
closed circle, indicate mean iodine intake on the order of 200 μg d-1, suggesting a ratio Y/Sgreater than the baseline value 2.5. The transfer coefficient based on the ratio Y/S = 3 isconsistent with mean 2-hour thyroidal uptake for that group.
(239) Model predictions of the percentage U of ingested radioiodine in the thyroid at 24 hafter intake assuming no radioactive decay are compared in Figure 5-5 with observed values
for subjects with different levels E of stable iodine in urine. Model predictions are based on
the transfer coefficients in Table 5-1 except that the transfer coefficient from Blood 1 toThyroid 1 was varied with E as described by Eq. 5-3 down to a minimum value of 2.5 d-1.
For this comparison the value S was set at the gender-averaged reference value of 64 μg d-1.
(240) The model with baseline parameter values predicts that the thyroid contains about
29% of ingested or intravenously injected iodine at 24 h after intake, assuming no radioactive
decay. The content of the thyroid is predicted to peak at about 30% of the ingested or injectedamount during the period 24-48 h after intake.

77

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3021
3022
3023
3024

Figure 5-3. Model predictions of clearance of intravenously injected radioiodine from plasmacompared with central values determined in three studies.

3025
3026
3027
3028

Figure 5-4. Model predictions of thyroidal uptake of intravenously injected 131I compared withmean values of external measurements for three study groups.

78

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

3029
3030
3031
3032
3033
3034
3035
3036
3037
3038
3039
3040
3041
3042
3043

Figure 5-5. Model predictions and observations of 24-h uptake of radioiodine by thyroid (U) as
a function of daily urinary excretion of stable iodine (E). After Leggett (2010).

(241) Model predictions of the equilibrium content of iodine in the thyroid, concentrationof inorganic iodide and organic iodine in blood, and total extrathoracic contents of inorganic
iodide and organic iodide are listed in Table 5-5 for different combinations of dietary iodine
Y and thyroidal secretion rate S. The predicted values for each of these quantities based onreference values for dietary stable iodine Y and secretion rate of hormonal iodine S for
women, total adult population, and men (see the first three columns of model predictions) arewithin the ranges of reported values for euthyroid subjects. For example, predictions of themass of iodide in the thyroid at equilibrium are 6.00, 7.39, and 8.77 g, compared with typicalvalues of 5-15 mg. Predictions of the concentration of organic iodine in blood plasma are
3.9-5.8 μg/dl, compared with commonly reported values of 3-8 μg/dl.
Table 5-5. Model predictions of mass or concentration of iodine in tissues and fluids atequilibrium

Quantity
Iodine in thyroid (μg)
Iodide in blood plasma (μg dl-1)
Total extrathyroidal inorganic iodide (μg)
Organic iodine in blood plasma (μg dl-1)
Total extrathyroidal organic iodine (μg)
a

b

3044
3045
3046
3047

Dietary iodine(μg d-1) /Thyroidal secretion of organic iodine (μg d-1)
130 / 52a 160 / 64a 190 / 76a 300 / 100b
6750
8310
9870
13,000
0.22
0.27
0.32
0.51
58
71
84
135
4.3
5.2
6.2
8.2
520
640
760
1000

Baseline transfer coefficient describing thyroidal uptake (7.26 d-1) is applied because the ratio of
daily intake of iodine Y to daily thyroidal secretion S is 2.5.
Transfer coefficient from Blood iodide to Thyroid iodide is 5.96 d-1 based on Eq. 5-2.

5.2.3.3. Treatment of radioactive progeny(242) Chain members addressed in the derivation of dose coefficients for iodine isotopes
79

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3048
3049
3050
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3053
3054
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3066
3067
3068
3069
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3073
3074
3075
3076
3077
3078
3079
3080
3081
3082
3083
3084
3085
3086
3087
3088
3089
3090
3091
3092
3093
3094
3095

are isotopes of iodine, tellurium, antimony, or xenon. Tellurium, antimony, or iodine atoms
produced in systemic compartments are assumed to follow the characteristic models for theseelements (i.e. the models applied in this report to these elements as parent radionuclides) fromtheir time of production. The implementation of this assumption is not always
straightforward. In some cases, the site of production of antimony or tellurium may not beclearly identifiable with a specific compartment in its characteristic biokinetic model due todifferences in model structures for the different elements. In such cases a transfer rate fromthe site of production of the radionuclide to the central blood compartment in theradionuclide’s characteristic model has been assigned as described below. After reaching its
central blood compartment, the radionuclide is assumed to behave as described by its
characteristic model.
(243) Tellurium atoms produced in the blood iodide compartment of the iodine model are
assigned to the central blood compartment of the tellurium model. Tellurium atoms producedin the blood organic iodine compartment of the iodine model are assumed to transfer to thecentral blood compartment of the tellurium model at the rate 1000 d-1. Tellurium atoms
produced at soft-tissue sites in the iodine model are assumed to transfer to the central bloodcompartment of the tellurium model at the rate 0.0693 d-1 (half-time of 10 d), which is therate of removal from all soft tissue compartments in the characteristic model for tellurium.
(244) Antimony produced in the blood iodide compartment of the characteristic model for
iodine or the central blood compartment of the characteristic model for tellurium is assigned
to the central blood compartment of the characteristic model for antimony. Antimony
produced in another blood compartment of the iodine or tellurium model is assumed totransfer to the central blood compartment of the antimony model at the rate 1000 d-1.
Antimony produced at any soft-tissue site in the iodine or tellurium model is assumed totransfer to the central blood compartment of the antimony model at the rate 0.693 d-1 (halftime of 1 d), which is the highest rate of removal from all soft tissue compartments in thecharacteristic model for antimony. Antimony produced in a bone compartment of thetellurium model is assumed to behave as if entering that site as a parent radionuclide.
(245) A generic biokinetic model is applied in this report to xenon isotopes produced bydecay of radionuclides in systemic pools. Xenon produced in bone is assumed to transfer toblood at the rate 100 d-1 if produced in bone surface and 0.36 d-1 if produced in bone volume.
These rates are taken from the model for radon introduced in ICRP Publication 67 (1993).
Xenon produced in a soft-tissue compartment is assumed to transfer to blood with a half-timeof 20 min. Xenon produced in the blood inorganic iodide compartment is assigned to theblood compartment of the xenon model. Xenon produced in the blood organic iodine
compartment is assumed to transfer to blood in the xenon model at the rate 1000 d-1. Xenon
entering the blood compartment of the xenon model or produced in that compartment isassumed to be exhaled at the rate 1000 d-1.
5.3.

Individual monitoring

125I(246) Thyroid monitoring is generally used for the monitoring of 125 I. The urinary
excretion rate decreases rapidly with time following intake and so thyroid monitoring is to bepreferred until the actual time of intake is known.
(247) Ge detectors, in the thyroid counting configuration, should preferably be usedbecause of the low energy photon emission from 125I.

80

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
IsotopeMonitoring
Technique

125

I
I

Urine Bioassay
Urine Bioassay

I

Thyroid Counting

125

125

3096
3097
3098
3099
3100
3101
3102
3103

3104
3105
3106
3107
3108
3109
3110
3111
3112
3113
3114

of Typical
DetectionLimit
γ-ray spectrometry 1Bq/L
Liquid scintillation 1 Bq/L
counting
γ-ray spectrometry 40 Bq

Achievabledetection limit
0.4Bq/L

1 Bq

129

I
(248) Thyroid monitoring is generally used for the monitoring of 129 I. The urinary
excretion rate decreases rapidly with time following intake and so thyroid monitoring is to bepreferred unless the actual time of intake is known.
(249) Ge detectors, in the thyroid counting configuration, should preferably be usedbecause of the low energy photon emission from 129 I.
IsotopeMonitoring
Technique

129

I

129

I

MethodMeasurement

Achievabledetection limit

Urine Bioassay

of Typical
DetectionLimit
γ-ray spectrometry 1 Bq/L

Thyroid Counting

γ-ray spectrometry

8 Bq

40 Bq

0.5 Bq/L

131

I(250) In vivo monitoring of the thyroid is the preferential method of monitoring 131I
exposures. Iodine-131 can be readily detected using a NaI detector or a germanium detector
system. Urinary monitoring is also a reliable method of monitoring for radioiodine. The
urinary excretion rate decreases rapidly with time following intake and so thyroid monitoringis to be preferred unless the actual time of intake is known. Use of both measurements, where
feasible, can increase confidence in estimated doses.
(251) Although not common in routine monitoring, Whole Body Counting is also feasiblein special situations, as for example when thyroid is blocked.
Isotope
131
131

131

3115
3116
3117
3118
3119
3120
3121
3122
3123
3124

MethodMeasurement

I
I
I

Monitoring
Technique

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
γ-ray spectrometry
2 Bq/LThyroid Counting γ-ray spectrometry, 25 Bq
in vivo
Whole
Body γ-ray spectrometry, 70 Bq
Counting
in vivo

Achievabledetection limit
0.3 Bq/L
1 Bq
15 Bq

References
Acland, J. D. (1971). The interpretation of the serum protein-bound iodine: A review. J. Clin. Path.
24:187-218.
Adams, G. A.; Bonnell, J. A. (1962). Administration of stable iodide as a means of reducing thyroid
irradiation resulting from inhalation of radioactive iodine. Health Phys. 7:127-149.
Alexander, W. D.; Shimmins, J.; Robertson, J. W. K.; Horton, P. W.; McLarty, D. G.; Harden, R. M.
(1971). Radioisotope studies of thyroid function and thyroid hormone metabolism. In:

81

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3125
3126
3127
3128
3129
3130
3131
3132
3133
3134
3135
3136
3137
3138
3139
3140
3141
3142
3143
3144
3145
3146
3147
3148
3149
3150
3151
3152
3153
3154
3155
3156
3157
3158
3159
3160
3161
3162
3163
3164
3165
3166
3167
3168
3169
3170
3171
3172
3173
3174
3175

Dynamic studies with radioisotopes in medicine. Proceedings of a symposium. Rotterdam, 31
Aug – 4 Sept, 1970. IAEA, Vienna, 179-190.
Anbar, M.; Guttman, S.; Rodan, G.; Stein, J. A. (1965). The determination of the rate of deiodinationof thyroxine in human subjects. J. Clin. Invest. 44:1986-1991.
Bair, W. J. (1961) Deposition, retention, translocation and excretion of radioactive particles. IN
Inhaled Particles and Vapours (Edited by C.N. Davies) Pergamon Press, Oxford pp. 192-208.
Bazin, J. P.; Fragu, P.; Di Paola, R.; Di Paola, M.; Tubiana, M. (1981). Early kinetics of thyroid trap
in normal human patients and in thyroid diseases. Eur. J. Nucl. Med. 6:317-326.
Bercz, J.P., Jones, L. L., Harrington, R. M., Bawa, R., Condie, L. 1986. Mechanistic aspects ofingested chlorine dioxide on thyroid function: impact of oxidants on iodide metabolism
Environ.Health Perspect. 69, 249-254.
Berkovski, V. (1999a) Radioiodine biokinetics in the mother and fetus. Part 1. Pregnant woman. In:
Radiation and Thyroid Cancer. World Scientific Publishing. Publication No. EUR 18552 EN.
pp.319-325.
Berkovski, V. (1999b) Radioiodine biokinetics in the mother and fetus. Part 2. Fetus. In: Radiation
and Thyroid Cancer. World Scientific Publishing. Publication No. EUR 18552 EN. pp.327332.
Berkovski, V. (2002). New iodine models family for simulation of short-term biokinetics processes,
pregnancy and lactation. Food and Nutrition Bulletin 23:87-94.
Berman, M.; Hoff, E.; Barandes, M.; Becker, D. V.; Sonnenberg, M.; Benua, R.; Koutras, D. A.
(1968). Iodine kinetics in man – a model. J. Clin. Endocrinol. Metab. 28:1-14.
Berson, S. A.; Yalow, R. S. (1954). Quantitative aspects of iodine metabolism. The exchangeableorganic iodine pool, and the rates of thyroidal secretion, peripheral degradation and fecal
excretion of endogenously synthesized organically bound iodine. J. Clin. Invest. 33: 1533–
1552.
Berson, S. A.; Yalow, R. S. (1955). The iodide trapping and binding functions of the thyroid. J. Clin.
Invest. 34:186-204.
Berson, S. A.; Yalow, R. S.; Sorrentino, J.; Roswit, B. (1952). The determination of thyroidal andrenal plasma 131I clearance rates as a routine diagnostic test of thyroid dysfunction. J. Clin.
Invest. 31:141–158.
BEST (Board on Environmental Studies and Toxicology) (2005). Health implications of perchlorate
ingestion. Washington, DC: The National Academy Press.
Bianchi, R.; Zucchelli, G. C.; Giannessi, D. ; Pilo, A. ; Mariani, G. ; Carpi, A. ; Toni, M. G. (1978).
Evaluation of triiodothyronine (T3) kinetics in normal subjects, in hypothyroid, andhyperthyroid patients using specific antiserum for the determination of labeled T3 in plasma.
J. Clin. Endocrinol. Metab. 46:203-214.
Bianco, A. C.; Larsen, P. R. (2005). Intracellular pathways of iodothyronine metabolism. In: Wernerand Ingbar's The Thyroid: A Fundamental and Clinical Text, 9th edition, Werner, S. C.;
Ingbar, S. H.; Braverman, L. E.; Utiger, R. D., eds. New York: Lippincott Williams &Wilkins; pp. 109-134.
Bilek, R., Bednar, J.; Zamrazil, V. (2005). Spectrophotometric determination of urinary iodine by the
Sandell-Kolthoff reaction subsequent to dry alkaline ashing. Results from the Czech Republicin the period 1994-2002. Clin. Chem. Lab. Med. 43:573-580.
Black ,A., Hounam, R.F., 1968. Penetration of iodine vapour through the nose and mouth and theclearance and metabolism of the deposited iodine. Ann. Occup.Hyg. 11, 209-225.
Bohe, M., Borgstrom, A., Genell, S., and Ohlsson, K. (1986) Metabolism of 131I-labelled humanpancreatic cationic trypsin after intraduodenal administration. Digestion 34, 127-35.
Bordell, F. L.; Sayeg, J. A.; Wald, N. (1972). In vivo measured effective half-life of 125I in human
thyroids. Phys. Med. Biol. 17:365-373.
Bricker, N. S.; Hlad, C. J. (1955). Observations on the mechanism of the renal clearance of 131I. J.
Clin. Invest. 34:1057-1072.

82

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3176
3177
3178
3179
3180
3181
3182
3183
3184
3185
3186
3187
3188
3189
3190
3191
3192
3193
3194
3195
3196
3197
3198
3199
3200
3201
3202
3203
3204
3205
3206
3207
3208
3209
3210
3211
3212
3213
3214
3215
3216
3217
3218
3219
3220
3221
3222
3223
3224
3225
3226

Brownell, G. L. (1951). Analysis of techniques for the determination of thyroid function withradioiodine. J. Clin. Endocrinol. 11:1095-1105.
Burman, K. D. (2006). Low iodine diets. In: L. Wartofsky and D. Van Nostrand, Thyroid Cancer, A
comprehensive guide to clinical management, Second edition. Totowa, NJ: Human Press. pp.
677-681.
Busnardo, B.; Casson, F. (1965). Aspects of fecal iodine excretion in man. Acta. Isot. (Padova) 31:513.
Caldwell, K. L.; Jones, R.; Hollowell, J. G. (2005). Urinary iodine concentration: United States
National Health and Nutrition Examination Survey 2001-2002. Thyroid 15:692-699.
Cavalieri, R. R.; Searle, G. L. (1966). The kinetics of distribution between plasma and liver of 131Ilabeled L-thyroxine in man : Observations of subjects with normal and decreased serum
thyroxine-binding globulin. J. Clin. Invest. 45: 939-949.
Cavalieri, R. R.; Steinberg, M. ; Searle, G. L. (1970). The distribution kinetics of triiodothyronine:
Studies of euthyroid subjects with decreased plasma thyroxine-binding globulin and patientswith Graves' disease. J. Clin. Invest. 49:1041-1050.
CDC (2008). U.S. Centers for Disease Control and Prevention: National report on biochemical
indicators of diet and nutrition in the U.S. population 1999–2002. Available from:http://www.cdc.gov/nutritionreport/index.html.
Chopra, I. J. (1976). An assessment of daily production and significance of thyroidal secretion of 3,3’,5’-triiodothyronine (reverse T3) in man. J. Clin. Invest. 58:32-40.
Choufoer, J. C.; van Rhijn, M.; Kassenaar, A. A.; Querido, A. (1963). Endemic goiter in Western
New Guinea: Iodine metabolism in goitrous and nongoitrous subjects. J. Clin. Endocrinol.
Metab. 23:1203-1218.
Cohn, B. N. E. (1932). Absorption of compound solution of iodine from the gastro-intestinal tract.
Arch. Intern. Med. 49:950-956.
Coughtrey, P., Jackson, D. and Thorne, M. (1983) Radionuclide distribution and transport interrestrial and aquatic ecosystems. Vol. 3. A.A. Balkema, Rotterdam. pp.341-346.
Dadachova, E.; Bouzahzah, B.; Zuckier, L. S.; Pestell, R. G. (2002). Rhenium-188 as an alternative toiodine-131 for treatment of breast tumors expressing the sodium/iodide symporter (NIS).
Nucl. Med. Biol. 29:13-18.
Dawson, C. A., Skebba, S. C., Lineham, J. H. and Bronikowski, T. A. (1985) Influence of pulmonary
embolism on absorption of inhaled iodide-125. J. Appl. Physiol. 58, 1061-1068.
Degon, M.; Chipkin, S.; Hollot, C. V.; Zoeller, T.; Chait, Y. (2008). A computational model of thehuman thyroid. Math Biosci. 212:22-53.
DeGroot, L. J.; Decostre, P.; Phair, R. (1971). A mathematical model of human iodine metabolism. J.
Clin. Endocr. 32:757-765.
Delange, F. M.; Dunn, J. T. (2005). Iodine deficiency. In: Werner and Ingbar's The Thyroid: A
Fundamental and Clinical Text, 9th edition, Werner, S. C.; Ingbar, S. H.; Braverman, L. E.;
Utiger, R. D., eds. New York: Lippincott Williams & Wilkins; pp. 264-288.
Dunning, D. E.; Schwarz, G. (1981).Variability of human thyroid characteristics and estimates ofdose from ingested 131I. Health Phys. 40:661-675.
Ermans, A. M. (1993). Iodine kinetics in iodine deficiency. In: Delange, F.; Dunn, J. T.; Glinoer, D.,eds. Iodine deficiency in Europe: A continuing concern. New York: Plenum; pp. 51-56.
Esposito, E. J. (1970). 131I concentration in submaxillary glands and other tissues of rats. J. Dent. Res.
49:459.
FAO/WHO (2002). Chapter 12. Iodine. In: Human vitamin and mineral requirements. Report of a
joint FAO/WHO expert consultation. Bangkok, Thialand. Food and Agriculture Organizationof the United Nations.World Health Organization. Update of March 12, 2002. pp. 181-194.
Fisher, D. A.; Oddie, T. H. (1969a). Thyroidal radioiodine clearance and thyroid iodine
accumulation: Contrast between random daily variation and population data. J. Clin.
Endocrinol. Metab. 29:111-115.

83

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3227
3228
3229
3230
3231
3232
3233
3234
3235
3236
3237
3238
3239
3240
3241
3242
3243
3244
3245
3246
3247
3248
3249
3250
3251
3252
3253
3254
3255
3256
3257
3258
3259
3260
3261
3262
3263
3264
3265
3266
3267
3268
3269
3270
3271
3272
3273
3274
3275
3276
3277
3278

Fisher, D. A.; Oddie, T. H. (1969b). Comparison of thyroidal iodine content and turnover in euthyroid
subjects: Validity of estimation of thyroid iodine accumulation from short-term clearance
studies. J. Clin. Endocrinol. Metab. 29:721-727.
Fisher, D. A.; Oddie, T. H.; Epperson, D. (1965). Effect of increased dietary iodide on thyroid
accumulation. J. Clin. Endocrinol. Metab. 25:1580-1590.
Fisher, D. A.; Oddie, T. H.; Thompson, C. S. (1971). Thyroidal thyronine and non-thyronine iodine
secretion in euthyroid subjects. J. Clin. Endocrinol. Metab. 33:647-652.
Greenspan, F. S. (2004). The thyroid gland. Chapter 7 in: Greenspan, F. S.; Gardner, D. G. Basic andclinical endocrinology, seventh edition. New York: McGraw-Hill.
Gregerman, R. I.; Gaffney, G. W.; Schock, N. W. (1962). Thyroxine turnover in euthyroid man withspecial reference to changes with age. J. Clin. Invest. 41:2065-2074.
Halnan, K. E. (1964). The metabolism of radioiodine and radiation dosage in man. Brit. J. Radiol.
37:101-114.
Handl, J.; Kuehn, W.; Hesch, R. D. (1984). Content and heterogeneity of distribution of iodine inhuman and bovine thyroid glands determined by neutron activation analyses. J. Endocrinol.
Invest. 7:97-101.
Harden, R. M.; Alexander, W. D. (1968). The salivary iodide trap in man: Clinical applications. Proc.
R. Soc. Med. 61:647–649.
Harden, R. M.; Alexander, W. D.; Shimmins, J.; Chisholm, D. (1969). A comparison between thegastric and salivary concentration of iodide, pertechnetate, and bromide in man. Gut 10:928930.
Harrison, M. T. (1968). Iodine balance in man. Postgrad. Med. J. 44:69-71.
Hays, M. T. (1985). Radiation dosimetry of radioiodinated thyroid hormones. J. Nucl. Med. 25:10681074.
Hays, M. T. (2001). Estimation of total body iodine content in normal young men. Thyroid 7:671675.
Hays, M. T.; McGuire, R. A. (1980). Distribution of subcutaneous thyroxine, triiodothyronine, andalbumin in man : Comparison with intravenous administration using a kinetic mode. J. Clin.
Endocrinol. Metab. 51:1112-1117.
Hays, M. T.; Solomon, D. H. (1965). Influence of the gastrointestinal iodide cycle on the early
distribution of radioactive iodide in man. J. Clin. Invest. 44:117-127.
Hays, M. T.; Solomon, D. H. (1969). Effects of epinephrine on the peripheral metabolism of
thyroxine. J. Clin. Invest. 48:1114-1123.
Hays, M. T.; Wegner, L. H. (1965). A mathematical and physiological model for early distribution ofradioiodine in man. J. Appl. Physiol. 20:1319-1328.
Hellstern, P.; Keller, H. E.; Weinheimer, B.; Wesch, H. (1978). Thyroid iodine concentration andtotal thyroid iodine in normal subjects and in endemic goiter subjects. Clin. Endocrinol.
9:351-356.
Herrmann, J,; Heinen, E.; Kroll, H. J.; Rodorff, K. H.; Krueskemper, H. L. (1981) Thyroid function
and thyroid hormone metabolism in elderly people. Klin. Wochenschr. 59:315-323.
Hiss, J. M.; Dowling, J. T. (1962). Thyroxine metabolism in untreated and treated pancreatic
steatorrhea. J. Clin. Invest. 41:988-995.
ICRP (1979) International Commission on Radiological Protection. Limits on Intakes ofRadionuclides for Workers. ICRP Publication 30, Pt.1. Pergamon Press, Oxford. Ann. ICRP
2, (3/4).
ICRP (1987). International Commission on Radiological Protection. Radiation dose to patients fromradiopharmaceuticals. ICRP Publication 53. Oxford: Pergamon Press.
ICRP (1989) International Commission on Radiological Protection. Age-dependent Doses toMembers of the Public from Intake of Radionuclides. Pt.1. ICRP Publication 56. Pergamon
Press, Oxford. Ann. ICRP 20, (2).
ICRP, 1993. Age-dependent Doses to Members of the Public from Intake of Radionuclides: Part 2,
Ingestion Dose Coefficients, ICRP Publication 67. Annals of the ICRP 23 (3/4).

84

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3279
3280
3281
3282
3283
3284
3285
3286
3287
3288
3289
3290
3291
3292
3293
3294
3295
3296
3297
3298
3299
3300
3301
3302
3303
3304
3305
3306
3307
3308
3309
3310
3311
3312
3313
3314
3315
3316
3317
3318
3319
3320
3321
3322
3323
3324
3325
3326
3327
3328
3329

ICRP (1994). International Commission on Radiological Protection. Dose coefficients for intakes ofradionuclides by workers, ICRP Publication 68. Oxford: Pergamon Press.
ICRP (1997). International Commission on Radiological Protection. Individual monitoring forinternal exposure of workers. Replacement of ICRP Publication 54. ICRP Publication 78.
Oxford: Pergamon Press.
ICRP (2002a) Guide for the Practical Application of the ICRP Human Respiratory Tract Model.
Supporting Guidance 3. Annals of the ICRP, 32(1-2).
ICRP (2002b). International Commission on Radiological Protection. Basic anatomical andphysiological data for use in radiological protection: Reference values. ICRP Publication 89.
Oxford: Pergamon Press.
ICRP (2006). International Commission on Radiological Protection. Human alimentary tract model
for radiological protection. ICRP Publication 100. Oxford: Pergamon Press.
Inada, M.; Kasagi, K.; Kurata, S.; Kazama, Y.; Takayama, H.; Torizuka, K.; Fukase, M.; Soma, T.
(1975). Estimation of thyroxine and triiodothyronine distribution and of the conversion rateof thyroxine to triiodothyronine in man. J. Clin. Invest. 55:1337-1348.
Ingbar, S. H.; Freinkel, N. (1955). Simultaneous estimation of rates of thyroxine degradation andthyroid hormone synthesis. J. Clin. Invest. 34:808-819.
Iyengar, G. V.; Kawamura, H.; Dang, H. S.; Parr, R. M.; Wang, J.; Akhter, P.; Cho, S. Y.; Natera, E.;
Miah, F. K.; Dojosubroto, J.; Nguyen, M. S. (2004). Dietary intakes of seven elements ofimportance in radiological protection by Asian population: Comparison with ICRP data.
Health Phys. 86:557–564.
Johansson, L.; Leide-Svegborn, S.; Mattsson, S.; Nosslin, B. (2003). Biokinetics of Iodide in Man:
Refinement of Current ICRP Dosimetry Models. Cancer Biotherapy andRadiopharmaceuticals 18:445-450.
Johnson, J. R. (1987). A review of age dependent radioiodine dosimetry. In: Gerber, G. B.; Metivier,
H.; Smith, H., eds. Age-related factors in radionuclide metabolism and dosimetry. Dordrecht:
Martinus Nijhoff Publishers; pp. 249-260.
Keating, F. R., Jr.; Albert, A. (1949). The metabolism of iodine in man as disclosed with the use ofradioiodine. Recent Progr. Hormone Research 4:429-481.
Kirchgessner, M.; He, J.; Windisch, W. (1999). Homeostatic adjustments of iodine metabolism andtissue iodine to widely varying iodine supply in 125I labeled rats. J. Anim. Physiol. Anim.
Nutr. 82:238-250.
Kolbert, K. S.; Pentlow, K. S.; Pearson, J. R.; Sheikh, A.; Finn, R. D.; Humm, J. L.; Larson, S. M.
(2007). Prediction of absorbed dose to normal organs in thyroid cancer patients treated with131
I by use of 124I PET and 3-dimensional internal dosimetry. Software. J. Nucl. Med.
48:143–149.
Kopp, P. (2005). Thyroid hormone synthesis. In: Werner and Ingbar's The Thyroid: A Fundamental
and Clinical Text, 9th edition, Werner, S. C.; Ingbar, S. H.; Braverman, L. E.; Utiger, R. D.,
eds. New York: Lippincott Williams & Wilkins; pp. 52-76.
Korolev, G. K. (1969). Distribution of iodine-132 and tellurium-132 in the body of rats under
intravenous administration. In: Moskalev, Yu. I., ed. Radioactive isotopes and the body.
Izdatel’stvo Meditsina. AEC-tr-7195; pp. 175-185.
Koutras, D. A.; Alexander, W. D.; Harden, R. M.; Wayne, E. (1964). Effect of small iodine
supplements on thyroid function in normal individuals. J. Clin. Endocrinol. Metab. 24:857862.
Lake-Bakaar, G., Rubio, C. E., McKavanagh, S., Potter, B. J., and Summerfield, J. A. (1980)
Metabolism of 125I-labelled trypsin in man: evidence of recirculation. Gut 21, 580-6.
Leggett, R. W. (2010). A physiological systems model for iodine for use in radiation protection.
Radiation Research 174: 496-516.
Lennon, E. J.; Engbring, N. H.; Engstrom, W. W. (1961). Studies of the rate of disappearance oflabeled thyroxine from the intravascular compartment. Clin. Invest. 40:996-1005.

85

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3330
3331
3332
3333
3334
3335
3336
3337
3338
3339
3340
3341
3342
3343
3344
3345
3346
3347
3348
3349
3350
3351
3352
3353
3354
3355
3356
3357
3358
3359
3360
3361
3362
3363
3364
3365
3366
3367
3368
3369
3370
3371
3372
3373
3374
3375
3376
3377
3378
3379
3380

Mariotti, S.; Franceschi, C.; Cossarizza, A.; Pinchera, A. (1995). The aging thyroid. Endocrine
Reviews 16:686-715.
McClellan, R. O. and Rupprecht, F. C. (Editors) (1968) Radioiodine metabolism in the beagle dog The importance of age and mode of 131I exposure. Fission Product Inhalation Program
Annual Report 1967-1968, LF-39, pp. 122-127. Lovelace Foundation for Medical Education
and Research, Albuquerque, New Mexico. Available from National Technical Information
Service, Springfield, Virginia.
McGuire, R. A.; Hays, M. T. (1981). A kinetic model of human thyroid hormones and theirconversion products. J. Clin. Endocrinol. Metab. 53:852-862.
Milakovic, M.; Berg, G.; Nystro, E.; Lindstedt, G.; Gebre-Medhin, M. (2004). Urinary iodine andthyroid volume in a Swedish population. J. Internal Med. 255:610–614.
MIRD (1975). MIRD dose estimate report no. 5. Summary of current radiation dose estimates tohumans from 123I, 124I, 125I, 126I, 130I, 131I, and 132I as sodium iodide. J. Nucl. Med. 16:857-860.
Mirell, S. G., Blahd, W. H. (1989). Biological retention of fission products from the Chernobyl
plume. Health Phys. 57 (4), 649-52.
Mithen, R. (2007) Effect of genotype on micronutrient absorption and metabolism: a review of iron,copper, iodine and selenium, and folates. Int J Vitam Nutr Res 77, 205-16.
Morgan, A., Morgan D. J. and Black, A. (1968a) A study of the deposition translocation andexcretion of radioiodine inhaled as iodine vapour. Health Phys., 15, 313-322.
Morgan, A., Morgan, D. J. and Arkell, G. M. (1967b) A study of the retention and subsequent
metabolism of inhaled methyl iodide. In: Inhaled Particles and Vapours II (C. N. Davies,
Ed.) Pergamon Press, Oxford pp. 309-321.
Morgan, A., Morgan, D. J., Evans, J. C. and Lister, B. A. J. (1967a) Studies on the retention andmetabolism of inhaled methyl iodide - II. Metabolism of methyl iodide. Health Phys. 13,
1067-1074.
Morgan, D. J. and Morgan, A. (1967) Studies on the retention and metabolism of inhaled methyl
iodide - I. Retention of inhaled methyl iodide. Health Phys. 13, 1055-1065.
Morgan, D. J., Black, A., Mitchell, G. (1968b) Retention of inhaled ethyl iodide labeled with iodine132.
Nature, 218 (5147), 1177-1178.
Morrow, P. E., Gibb, F. R., Davies, H. and Fisher, M. (1968) Dust removal from the lungparenchyma: an investigation of clearance stimulants. Toxicol. Appl. Pharmacol. 12, 372396.
Moskalev, Yu. I.; Yegorova, G. M. (1972). Distribution of iodine-131 in the rat organism following
separate and combined exposure to this isotope and cobalt-60 gamma rays. In: Moskalev, Yu.
I.; Kalistratova, V. S., eds. Biological effects of radiation from external and internal sources.
Meditsina. AEC-tr-7457; pp. 116-122.
Myant, N. B.; Corbett, B. D.; Honour, A. J.; Pochin, E. E. (1950). Distribution of radioiodide in man.
Clin. Sci. 9:405-419; 1950.
Nagataki, S.; Shizume, K.; Nakao, K. (1967). Thyroid function in chronic excess iodide ingestion:
Comparison of thyroidal absolute iodine uptake and degradation of thyroxine in euthyroid
Japanese subjects. J. Clin. Endocr. 27:638-647.
Nicoloff, J. T.; Dowling, J. T. (1968). Estimation of thyroxine distribution in man. J. Clin. Invest.
47:26-37.
Nicoloff, J. T.; Low, J. C.; Dussault, J. H.; Fisher, D. A. (1972). Simultaneous measurement of
thyroxine and triiodothyronine peripheral turnover kinetics in man. J. Clin. Invest. 51:473483.
Oddie, T. H.; Meschan, I.; Wortham, J. (1955). Thyroid function assay with radioiodine. I.
Physical basis of study of early phase of iodine metabolism and iodine uptake. J. Clin. Invest.
34: 95–105.
Oddie, T. H.; Fisher, D. A.; Epperson, D. (1965). Effect of exogenous thyroxine on thyroid
accumulation and secretion in euthyroid subjects. J. Clin Endocrinol. Metab. 25:1196-1206.

86

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3381
3382
3383
3384
3385
3386
3387
3388
3389
3390
3391
3392
3393
3394
3395
3396
3397
3398
3399
3400
3401
3402
3403
3404
3405
3406
3407
3408
3409
3410
3411
3412
3413
3414
3415
3416
3417
3418
3419
3420
3421
3422
3423
3424
3425
3426
3427
3428
3429
3430
3431

Oddie, T. H.; Fisher, D. A.; Long, J. M. (1964). Factors affecting the estimation of iodine entering thenormal thyroid gland using short-term clearance studies. J. Clin Endocrinol. Metab. 24:924933.
Oddie, T. H.; Fisher, D. A.; McConahey, W. M.; Thompson, C. S. (1970). Iodine intake in the UnitedStates: A reassessment. J. Clin Endocrinol. Metab. 30:659-665.
Oddie, T. H.; Meade, J. H.; Fisher, D. A. (1966). An analysis of published data on thyroxine turnoverin human subjects. J. Clin. Endocrinol. Metab. 26:425-436.
O’Hare, N. J.; Murphy, D.; Malone, J. F. (1998). Thyroid dosimetry of adult European populations.
Brit. J. Radiol. 71:535-543.
Ohtaki, S.; Moriya, S.; Suzuki, H.; Horiuchi, Y. (1967). Nonhormonal iodine escape from the normal
and abnormal thyroid gland.
Oppenheimer, J. H.; Bernstein, G.; Hasen, J. (1967).Estimation of rapidly exchangeable cellularthyroxine from the plasma disappearance curves of simultaneously administered thyroxine-I131 and albumin-I-125. J. Clin. Invest. 46:762-777.
Parr, R. M.; Crawley, H.; Abdulla, M; Iyengar, G. V.; Kumpulainen, J. (1992). Human dietary intakesof trace elements: A global literature survey mainly for the period 1970–91. Data listing andreferences. Report International Atomic Energy Agency (IAEA). Vienna: IAEA; IAEAHAHRES-12.
Pattle, R. E. (1961) The retention of gases and particles in the human nose. IN Inhaled Particles andVapours (Edited by Davies, C. N.) Pergamon Press, Oxford pp. 302-311.
Perrault, G., Thiéblemont, P., Pasquier, C. and Marblé, G. (1967) Cinétique du passage du radioiode
soluble à travers les épithéliums respiratoires, après inhalation. Health Phys. 13, 707-718.
Pittman, C. S.; Chambers, J. B.; Read, V. H. (1971). The extrathyroidal conversion rate of thyroxine
to triiodothyronine in normal man. J. Clin. Invest. 50:1187-1196.
Ramsden, D.; Passant, F. H.; Peabody, C. O.; Speight, R. G. (1967). Radioiodine uptakes in the
thyroid. Studies of the blocking and subsequent recovery of the gland following theadministration of stable iodine. Health Phys. 13:633-646.
Riggs, D.S. (1952) Quantitative aspects of iodine metabolism. Pharmacol. Rev. 4, 284-370.
Robertson, J. S.; Gorman, C. A. (1976). Gonadal radiation dose and its genetic significance inradioiodine therapy of hyperthyroidism. J. Nucl. Med. 17:826-835.
Robertson, J. W. K.; Shimmins, J.; Horton, P. W.; Lazarus, J. H.; Alexander, W. D. (1971).
Determination of the rates of accumulation and loss of iodide and of protein binding of iodinein the human thyroid gland. In: Dynamic studies with radioisotopes in medicine. Proceedingsof a symposium. Rotterdam, 31 Aug – 4 Sept, 1970. IAEA, Vienna, 199-210.
Ruegamer, W. R. (1953). The kinetics of 131I metabolism in the dog and human. Arch. Biochem.
Biophys. 47:119-136.
Sawin, C. (2005). Age-related changes in thyroid secretion. In: Werner and Ingbar's The Thyroid: A
Fundamental and Clinical Text, 9th edition, Werner, S. C.; Ingbar, S. H.; Braverman, L. E.;
Utiger, R. D., eds. New York: Lippincott Williams & Wilkins; pp. 214-219.
Shapiro, B.; Shulkin, B.; Gross, M.; Troncone, L. (1994). Thyroid imaging withradiopharmaceuticals. In: Troncone, L. Shapiro, B.; Satta, M.; Monaco, F. Thyroid Diseases.
Basic Science, Pathology, Clinical and Laboratory Diagnoses. CRC Press: 274-292.
Small, M. D.; Bezman, A.; Longarni, A. E.; Fennell, A.; Zamcheck, N. (1961). Absorption ofpotassium iodide from gastro-intestinal tract. Proc. Soc. Exp. Biol. Med. 106:450-452.
Smyth, P. P. A.; Duntas, L. H. (2005). Iodine uptake and loss – Can frequent strenuous exercise
induce iodine deficiency? Horm. Metab. Res. 37:555-558.
Stanbury, J. B.; Brownell, G. L.; Riggs, D. L.; Perinetti, H.; Itoiz, J.; del Castillo, E. B. Endemic
goiter. The adaptation of man to iodine deficiency. Cambridge, MA. Harvard University
Press. 1954.
Stather, J.W.; Greenhalgh, J.R. (1983). The metabolism of iodine in children and adults. National
Radiological Protection Board report NRPB-R140. Chilton, Didcot, June 1983.

87

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3432
3433
3434
3435
3436
3437
3438
3439
3440
3441
3442
3443
3444
3445
3446
3447
3448
3449
3450
3451
3452
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3455
3456
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3459
3460
3461
3462
3463
3464
3465
3466
3467
3468
3469
3470
3471
3472
3473
3474
3475
3476
3477
3478
3479
3480
3481
3482

Sterling, K. (1958). Radiothyroxine turnover studies in thyroid disease after therapy. J. Clin. Invest.
37:1348-1356.
Sterling, K.; Lashof, J. C.; Man, E. B. (1954). Disappearance from serum of I-131-labeled Lthyroxine and L-triiodothyronine in euthyroid subjects. J Clin Invest. 33:1031–1035.
Thiéblemont, P., Marblé, G., Perrault, G. and Pasquier, C. (1965a) Évaluation de la rétention
respiratoire et de l'élimination du radioiode après contamination aérienne du singe. Int. J.
Rad. Biol. 9, 219-231.
Thiéblemont, P., Marblé, G., Perrault, G. and Pasquier, C. (1965b) Charge thyroïdienne en radioiode
après contamination respiratoire du singe Macaccus rhesus. Int. J. Rad. Biol. 9, 233-240.
Thomas, R. L., Scott, J. K. and Chiffelle, T. L. (1970) Metabolism and toxicity of inhaled andinjected 131I in the rat. Amer. Ind. Hyg. Assn. J. 31, 213-220.
Tucker, R. G.; Keys, A. (1951). Concentration of serum protein-bound iodine in normal men. J. Clin.
Invest. 30:869-873.
Ulmer, D. D.; Perkins, L. B.; Kereiakes, J. G. (1959). Alterations in iodine-131 distribution in the rat
after whole-body x-irradiation. Radiat. Res. 11:810-819.
Underwood J. (1971). Iodine. In: Trace Elements in Human and Animal Nutrition. Academic Press,
New York.
Underwood, E.J. (1977). Iodine. In: Trace elements in human and animal nutrition, 4th edition,
Academic Press, New York, Chapter 11.
Utiger, R. D. (2001). Thyroid Diseases. In: Endocrinology and Metabolism, 4th edition, Felig, P.;
Frohman, L. A., eds. New York: McGraw-Hill; pp. 259-348.
Vadstrup S. (1993). Comparative aspects of iodine conservation in mammals. Comp. Biochem.
Physiol. 106A:15-17.
Wartofsky, L.; Martin, D.; Earll, J. M. (1972). Alterations in thyroid iodine release and the peripheral
metabolism of thyroxine during acute falciparum malaria in man. J. Clin. Invest. 51:22152232.
Wayne, E. J.; Koutras, D. A.; Alexander, W. D. (1964). Clinical aspects of iodine metabolism.
Philadelphia, PA: F. A. Davis Co.
Wellman, H. N.; Kereiakes, J. G.; Branson, B. M. (1970). Total- and partial-body counting ofchildren for radiopharmaceutical dosimetry data. In: Cloutier, R. J.; Edwards, C. L.; andSnyder, W. S., eds., Medical Radionuclides: Radiation Dose and Effects. U.S. Atomic
Energy Commission, Oak Ridge, TN; pp. 133-156.
WHO (1989). Iodine. In: Toxicological evaluation of certain food additives and contaminants. WHO
Food Additives Series, No. 24. World Health Organization. Cambridge, UK: Cambridge
University
Press.
No.
661
on
INCHEM.
Available
onlineat
http://www.inchem.org/documents/jecfa/jecmono/v024je11.htm.
WHO (2001). Assessment of the iodine deficiency disorders and monitoring their elimination. Second
edition. Joint publication of International Council for Control of Iodine Deficiency Disorders,
United Nations Children’s Fund, and World Health Organization (WHO). WHO/NHD/01.1.
Geneva: World Health Organization.
WHO (2004). Iodine status worldwide. WHO global database on iodine deficiency. de Benoist, B.;
Andersson, M.; Egli, I.; Takkouche, B.; Allen, H., eds. Geneva: Department of Nutrition for
Health and Development, World Health Organization.
Willard, D.H. and Bair, W.J. (1961) Behaviour of 131I following its inhalation as a vapour and as aparticle. Acta Radiol. 55, 486-496.
Winder, W. W.; Heninger, R. W. (1971). Effect of exercise on tissue levels of thyroid hormones in
the rat. Am. J. Physiol. 221:1139-1143.
Zanzonico, P. B.; Becker, D. V. (2000) Effects of time of administration and dietary iodine levels on
potassium iodide (KI) blockade of thyroid irradiation by 131I from radioactive fallout. HealthPhys. 78:660-667.

88

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
3483
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3488

Zuckier, L. S.; Dohan, O.; Li, Y.; Chang, C. J.; Carrasco, N. ; Dadachova, E. (2004). Kinetics ofperrhenate uptake and comparative biodistribution of perrhenate, pertechnetate, and iodide by
NaI symporter-expressing tissues in vivo. J. Nucl. Med. 45:500-507.
Zvonova, I. A. (1989). Dietary intake of stable I and some aspects of radioiodine dosimetry. HealthPhys. 57:471-475.

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6.
6.1.

Chemical Forms in the Workplace(252) Caesium is an alkali metal only present in oxidation state I. It behaves similarly topotassium in the body. Caesium may be encountered in industry in a variety of chemical andphysical forms, including soluble inorganic salts (chloride, nitrate) and less soluble sulphate.
134
Cs and 137Cs are important fission products and could also be encountered in relatively
insoluble fragments of irradiated fuel. 137Cs is commonly used for medical applications ascaesium chloride.
Table 6-1. Isotopes of caesium addressed in this report
IsotopeCs-125
Cs-127
Cs-129
Cs-130Cs-131
Cs-132
Cs-134aCs-134m
Cs-135
Cs-135m
Cs-136
Cs-137aCs-138

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CAESIUM (Z = 55)

a

6.2.

Physical half-life
45 m
6.25 h32.06 h29.21 m9.689 d6.479 d2.064 y2.903 h2.3E+6 y
53 m
13.167 d
30.167 y33.41 mDecay mode
EC, B+
EC, B+
EC, B+
EC, B+, BEC
EC, B+, BB-, EC
IT
BIT
BBB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides
are given on accompanying electronic disk.

Routes of Intake

6.2.1. Inhalation
Absorption Types and parameter values(253) There is some information on the behaviour of inhaled caesium in man following
accidental intakes. Information is also available from experimental studies of caesium in ionicforms (chloride, nitrate), in irradiated fuel fragments and other contaminated dusts associatedwith nuclear facilities, and in fused aluminosilicate particles (FAP).
(254) Absorption parameter values and Types, and associated fA values for particulate
forms of caesium are given in Table 6-2.
Caesium chloride(255) Animal experiments have shown that caesium chloride (CsCl) is rapidly andcompletely absorbed from the respiratory tract following inhalation. Lie (1964) and Thomas(1969) observed that in mice, rats, and guinea pigs killed less than 20 minutes after a 10minute inhalation exposure to 137CsCl, nearly all the activity had left the lungs, suggesting anabsorption rate corresponding to a time of the order of 10 minutes, i.e. sr ~ 100 d-1. Stara

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(1965) similarly observed that in guinea pigs killed 20 minutes after inhalation of 137CsCl,
there had been rapid clearance from the lungs, and by 24 hours the biokinetics of 137Cs wereindistinguishable from those following intraperitoneal injection. Morrow et al. (1968)
measured a lung retention half time of 0.003 d (~4 minutes) following inhalation of 134CsCl
by dogs, giving fr ~1 and sr = 200 d–1. Boecker (1969a) noted that following inhalation of137
CsCl by dogs, the lung quickly became one of the tissues to exhibit a low concentration of137
Cs. It was estimated by the Task group from the results of another study in which 137CsCl
was inhaled by dogs (Boecker, 1969b) that lung retention at 32 days was <1% of the initiallung deposit (ILD).
(256) Cuddihy and Ozog (1973) deposited 137CsCl directly onto the nasal membranes of
Syrian hamsters and followed the biokinetics of the 137Cs for 4 hours. Analysis of the results
here gave values of fr ~1.0 and sr ~6 d–1 (t½ ~ 2 hours), slower than in the other studies,possibly because of the experimental techniques used, including the anaesthetic or slower
clearance from the nasal passage than from the lungs. Similar observations were made forstrontium and barium chlorides which were also administered by Cuddihy and Ozog (seeStrontium and Barium Sections).
(257) Hölgye and Malý (2002) followed urinary excretion of 137Cs for 370 days after
presumed accidental inhalation of the chloride by a worker. Analysis here showed that theresults can be well fit assuming Type F absorption, i.e. that absorption from the lungs is rapid
compared to transfer from systemic tissues to urine.
(258) Based on the results of the experiments outlined above, specific absorption
parameter values for caesium chloride were estimated here to be: fr = 1 and sr = 100 d-1(consistent with assignment to default Type F). However, although specific parameter values
for caesium chloride based on in vivo data are available, they are not adopted separately here.
The data are (with those for caesium nitrate) used as the basis for the default rapid dissolution
rate for caesium. Hence specific parameter values for caesium chloride would be the same as
default Type F caesium parameter values, and therefore caesium chloride is assigned to TypeF instead.
Caesium nitrate(259) Lie (1964) obtained similar results following inhalation of caesium nitrate by rats asfor caesium chloride, but few details were given. In rats killed immediately after a 10-minuteinhalation exposure, nearly all the activity had left the lungs, suggesting an absorption rate
corresponding to a time of the order of 10 minutes, i.e. sr ~ 100 d-1. In view of the few details
given, these data are judged to be an insufficient basis to provide specific absorption
parameter values and caesium nitrate is therefore assigned to Type F.
Caesium sulphate(260) Miller (1964) followed distribution and retention of 137Cs in two men following
accidental intake (presumed to be inhalation) of caesium sulphate. The distribution along the
body was unchanged between 9 and 285 days, implying that absorption from the lungs wascomplete before the first measurement on day 9, and indicating Type F behaviour. These data
are judged to be an insufficient basis to provide specific absorption parameter values andcaesium sulphate is therefore assigned to Type F.
Irradiated fuel fragments and other contaminated dusts associated with nuclear facilities.
(261) Studies have been conducted of caesium associated with irradiated fuel fragments,
including particles released from the Chernobyl accident, and other materials, more or less
91

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well defined, associated with various nuclear facilities. Such studies indicate that some of thecaesium is rapidly absorbed (within days), but a fraction may be retained with the particle
matrix and absorbed over a period of months or years. The results of most of these studies
indicate Type M behaviour overall, but some indicate Type F and two, partial Type S
behaviour.
Chernobyl(262) Mirell and Blahd (1989) made whole-body measurements of activity on seven people
from about two weeks to several months after exposure to the initial Chernobyl reactor
accident plume in Kiev, Ukraine. Biological retention half-times were similar for different
radionuclides (34 days for 137Cs) and different from those expected for systemic retention,
indicating that they were trapped in particles and metabolically inert, thus indicating Type M
rather than Type F behaviour.
(263) Kutkov (1998, 2000) reported that about 920 Chernobyl nuclear power plant workers
involved in emergency operations on 26-27 April 1986 were examined by means of asemiconductor whole body counter. For 15 of these, who were examined more than fivetimes in the period 40–800 days after the accident, the effective half-time of 137Cs retention in
the body ranged from 230 to 590 days with a mean of 360 ± 30 days, much greater than
expected for systemic 137Cs (about 110 days). With other information on the characteristics ofnuclear fuel particles dispersed in the accident, it was inferred that radionuclides such as 137Cs
were trapped in the uranium oxide matrix. Kutkov (1998) reported HRTM parameter values
for Chernobyl nuclear fuel particles as: sp = 4 d-1, spt = 100 d-1, st = 0.002 d-1 (and f1 = 0.002),
corresponding to fr = 0.04, sr = 104 d–1, and ss = 0.002 d–1, giving assignment to Type M.
However, these reports only summarise the results and little information was given on how
the parameter values were derived.
(264) Cuddihy et al. (1989) measured the in vitro dissolution of samples of particles
released from the Chernobyl accident for up to 60 days. For all radionuclides measured,
including 137Cs, 10% dissolved in a few hours, and the rest with a half-time of 160 days.
Hence fr = 0.1, sr ~10 d–1, and ss = 0.004 d–1, giving assignment to Type M.
(265) Kutkov and Komaritskaya (1996) measured the in vitro leaching (for 122 days) of137
Cs from particles taken from the Chernobyl Shelter. Results indicated fr ~ 0.3, sr ~0.04 d–1,
and ss = 0.002 d–1, giving assignment to Type M.
(266) To simulate particles produced in a reactor accident such as that at Chernobyl, Al
Rayyes et al. (1993) prepared UO2 particles labelled with 134Cs by condensation. In distilledwater, about 95% dissolved in a few hours, indicating Type F behaviour. However forparticles ‘matured’ in 10% O2 + 90% CO2, about 40% remained after 21 days, indicating
Type M behaviour.
Other workplace exposures(267) Hesp (1964) followed whole body retention of 137Cs for 300 days after accidental
inhalation by a worker, and also reported measurements in urine, and in the chest. Analysis
here showed that the results can be reasonably well fit assuming about 50% Type F and 50%
Type M absorption, i. e., fr is about 0.5, but there is insufficient information to determine srand ss (indicating assignment to Type M overall).
(268) The results of a human study in which in vivo measurements were made for over 2
years after accidental inhalation of irradiated uranium indicate Type F behaviour of thecaesium present, although measurements of other radionuclides (95Zr-Nb, 103Ru, and 144Ce)
indicated Type M or S behaviour (Rundo, 1965).
92

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(269) Raghavendran et al. (1978) followed whole body retention of 137Cs in 12 radiation
workers at the Bhaba Atomic Research Centre for between 72 and 456 days. Results wereconsistent with retention of systemic caesium, indicating Type F behaviour (assuming intake
by inhalation).
(270) Froning et al. (2004) followed whole body retention of 137Cs for 16 years after
accidental inhalation of high temperature reactor fuel element ash by a worker. Measurements
showed that the longest-lived component was concentrated in the thoracic region, suggesting
long term lung retention of a relatively insoluble component. The authors found that data up
to about 2000 days could be well represented by assuming 77% Type F and 23% Type S.
However, subsequent clearance was slower than predicted for default Type S. Analysis here 2
confirmed this assessment, which can be represented by fr = 0.77; sr = 100 d–1 and ss = 10–4.
Application here of the updated HRTM, which assumes longer retention in the AlveolarInterstitial region than the original HRTM (see OIR Part 1, Section 3.2.2) gave a better fit to
the measurements after 2000 days, but with a smaller 'insoluble' fraction retained, i.e. with ahigher value of fr (~0.9).
(271) Andrieu and Fatome (1979) studied the clearance of mixed fission and activation
products in ~1 µm graphite particles following controlled inhalation by a volunteer; data over
~7 years imply partial Type S behaviour for the 137Cs component.
(272) The biokinetics of 137Cs were followed for 6 months after intratracheal instillation
into rats of a suspension of residues from a reactor fuel cooling pond (Stradling et al., 1989).
Lung retention at 30 days was 2% ILD, giving assignment to Type F. However, insufficient
information was published to enable derivation of absorption parameter values.
(273) The biokinetics of 137Cs were followed for 6 months after intratracheal instillation
into rats of a complex radionuclide bearing dust from the ventilation grid of the reactor fuelhall of a nuclear power plant (Stradling et al., 1996, 1997). Absorption parameter values: fr =0.82; sr = 2.7 d–1 and ss = 1.4 10–3 d–1 derived by ICRP (2002a, Section E4.4), are consistent
with assignment to Type M.
(274) Kotrappa et al. (1977) measured in vitro the fractions of several radionuclides that
dissolved rapidly (within 6 hours) from air samples taken at five working areas in a nuclear
power plant. For 134+137Cs the fraction was between 98% (consistent with Type F) and 38%(indicating possibly Type M behaviour). Dua et al. (1987) measured the in vitro dissolutionof particles on an air sample from a reactor spent fuel bay for up to 200 days. For all
radionuclides measured, including 137Cs, ~40% dissolved with a half-time of 1.2 days, and therest with a half-time of 155 days. Hence fr = 0.4, sr ~0.6 d–1, and ss = 0.004 d–1, giving
assignment to Type M.
(275) Although specific absorption parameter values were derived from the results of one
in vivo study, the results from others indicate that the biokinetics of caesium in the forms
considered in this section are likely to vary markedly. Caesium associated with irradiated fuelfragments, and other unspecified contaminated dusts from nuclear facilities, is therefore
assigned to Type M.
Fused aluminosilicate particles (FAP)(276) FAP or “fused clay” particles have been extensively used as relatively insoluble
particles in inhalation studies, both of biokinetics and of radiation effects. A natural clay
mineral is labelled by ion exchange, and the labelled clay particles heated to about 1100˚C, toform aluminosilicate glass microspheres in which the label is incorporated. It has been shown2

Data kindly provided by Dr M. Schläger, Forschungszentrum Jülich.

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3682
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3684
3685

in several animal studies (mouse, rat, guinea pig and dog) that when caesium is incorporated
into FAP, a small fraction is rapidly absorbed from the lungs (fr ~0.1). The rest is absorbed
slowly, at rates of the order of 0.001 d–1 (Boecker et al., 1974; Snipes et al., 1983; Snipes andMcClellan, 1986). In most cases the results give assignment to Type M, but for the largest
particles (2.8 μm AMAD) used by Snipes et al. (1983) they give Type S. In view of thevariability of the results, and because inhalation exposure to caesium-labelled FAP is sounlikely, specific parameter values for it are not used here, nor is it assigned to a default
Type.
Rapid dissolution rate for caesium(277) Studies with caesium chloride and nitrate outlined above, give values of sr of about
100 d–1, which is applied here to all Type F forms of caesium.
Extent of binding of caesium to the respiratory tract(278) Evidence from the caesium chloride studies outlined above suggests that there is
probably little binding of caesium. It is therefore assumed that for caesium the bound state
can be neglected, i.e. fb = 0.0.
Table 6-2. Absorption parameter values for inhaled and ingested caesium
Absorption
parameter Absorption fromavaluesthe alimentaryfrsr (d–1) ss (d–1) tract, fA

Inhaled particulate materials
Default parameter valuesb,cAbsorption
Assigned forms
Type
F
Caesium chloride, nitrate, sulphate 1
M
Irradiated fuel fragments; all 0.2
unspecified formsd
S—
0.01
Ingested materials
Caesium chloride, nitrate, sulphate; all unspecified –compounds
Relatively insoluble forms (irradiated fuel –fragments)
3686
3687
3688
3689
3690
3691
3692
3693
3694
3695
3696
3697
3698
3699
3700

100
3

0.005

1
0.2

3

1x10-4

0.01

–

–

1

–

–

0.1

a

It is assumed that for caesium the bound state can be neglected, i.e. fb = 0.0. It is assumed that for caesium thebound state can be neglected, i.e. fb = 0.0. The value of sr for Type F forms of caesium (100 d–1) is elementspecific. The values for Types M and S (3 d–1) are the general default values.
bMaterials (e.g. caesium chloride) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see text).
c
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type (or specific value where given) and the fA value for ingested soluble forms of caesium (1.0).
dDefault Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

6.2.2. Ingestion(279) Human volunteer studies using 137Cs in soluble inorganic form have shown virtually94

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3719
3720
3721
3722
3723
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3743
3744
3745
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3747
3748

complete absorption from the alimentary tract (Rosoff et al., 1963; Rundo et al., 1963;
Naversten and Liden, 1964; LeRoy et al., 1966). Thus, for example, Rundo et al. (1963)
measured an average fractional absorption of 0.99 for 10 normal subjects following theingestion of 137CsCl and Leroy et al. (1966) measured values from 0.87 to 0.9 on four healthy
subjects.
(280) 134Cs and 137Cs incorporated into insoluble particles may be less available forabsorption. LeRoy et al. (1966) reported values of 0.29-0.36 for 134Cs contained in
microspheres from leachable glass and ingested by three volunteers. These values were about
0.8 when 134Cs was given as caesium silicate to five volunteers.
(281) McKay and Memmott (1991) have shown that absorption of Cs adsorbed onto
inorganic sedimentary material was significantly lower than the unity. Experiment withanimals showed that absorption of 137Cs from irradiated reactor fuel particles (2 - 10 μm) in
adult rats were less than 0.1 (Talbot et al, 1993).
(282) In Publication 30 (ICRP, 1979), complete absorption from the alimentary tract was
assumed for all chemical forms of Cs. In this report, an fA of 1 is adopted for all forms of Cs,
except in situations where it is considered that the material is insoluble (e.g. fuel particles)
and a lower fA value of 0.1 is appropriate.
6.2.3. Systemic Distribution, Retention and Excretion
6.2.3.1. Summary of database(283) Caesium is a physiological analogue of the lighter alkali metals potassium andrubidium. Caesium has been shown to compete with these elements for both active andpassive membrane transport across cell membranes but is generally transported less readily
than potassium or rubidium by these processes (Hodgkin, 1947; Sjodin and Beauge, 1967;
Edwards, 1982; Latorre and Miller, 1983; Cecchi et al., 1987). In vitro studies of the relative
selectivity of potassium, caesium, and rubidium by membranes have revealed much about thestructure and functions of ionic channels and carriers.
(284) Numerous studies of the biological behavior of caesium in man and laboratory
animals have been published since the 1950s due to the importance of the fission-produced
isotopes 137Cs and 134Cs as occupational and environment hazards. The retention time of
caesium in the human body has been found to vary with age, gender, diet, muscle mass,pregnancy, and diseases that affect the behavior of potassium in the body. Studies onlaboratory animals indicate that absorbed caesium initially is heterogeneously distributed in
the body with highest concentration in the kidneys but gradually attains a more nearly
uniform distribution (Stather, 1970; Moskalev, 1972). Autopsy studies on environmentally
exposed humans indicate that caesium concentrations do not differ greatly for different
tissues, but higher concentrations generally are found in skeletal muscle than in othermeasured tissues (Yamagata, 1962; Williams and Leggett, 1987). Measurements on persons
briefly exposed to elevated levels of 137Cs in accidents or controlled studies show that wholebody retention for periods up to 3-4 years usually can be represented by the sum of two
exponential terms. The long-term component typically represents 85-95% of uptake in adults.
The long-term half-time generally is in the range 45-150 days in adults although values on theorder of 200 days have been reported (Rundo, 1964; Cryer and Baverstock, 1972; Lloyd et al.,1972, 1973; Leggett, 1986).
(285) Leggett et al. (1998) reviewed data on whole-body retention of caesium in healthy
adults from 14 studies involving 2-239 subjects per study. Central estimates of the long-term
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3769
3770
3771
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3777
3778
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3787
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3789
3790
3791
3792
3793
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3796

half-time in adult males were in the range 79-133 d with an overall mean of about 97 d. Intersubject variability within a given study generally was small, with a typical coefficient ofvariation of about 20% and a typical geometric standard deviation of about 1.2. In eight of the
14 studies, retention half-times were measured in both men and women. There was someoverlap in half-times for individual male and female subjects, but the mean half-time forfemales was 15-35% lower than that for males in each of the eight studies.
(286) The long-term half-time of cesium in the body usually is reduced during pregnancy
to about two-thirds of the value when not pregnant (Lloyd et al., 1966; Zundel et al., 1969;
Melo et al., 1997; Thornberg and Mattsson, 2000).
6.2.3.2. Biokinetic model for systemic caesium(287) In the model for systemic caesium adopted in ICRP Publication 30 (1979), caesiumis assumed to be uniformly distributed in the body at all times after uptake to blood. Wholebody retention at time t (days) is represented as a sum of two exponential terms:
R(t) = a exp(-0.693t/T1) + (1 - a) exp(-0.693t/T2),
where T1 and T2 are biological half-times for short-term and long-term components ofretention, respectively. Parameter values a = 0.1, T1 = 2 d, and T2 = 110 d are applied to theworker. This model is also applied in ICRP Publication 68 (1994), but explicit excretion
pathways are added: 80% of activity leaving the body is assumed to pass through the urinary
bladder contents to urine and 20% is assumed to be secreted into the upper large intestine andsubsequently excreted in faeces.
(288) The model for systemic caesium used in this report is adapted from a model
proposed by Leggett et al. (2003) that is constructed around a dynamic blood flow model
involving a number of different blood pools (Leggett and Williams, 1995; Leggett et al.,2006). The dynamic blood flow model is useful, for example, for predicting the blood
circulation and tissue accumulation of ultra-short-lived isotopes of caesium or its
physiological analogues (Leggett et al., 2006). For application to a caesium isotope with halflife of at least a few minutes, it suffices to treat blood plasma as a well-mixed centralcompartment. The latter form of the model is used in this report, with the following
modifications:
1. In the original model the skeleton is divided into two compartments representing red
marrow and all remaining skeletal tissues. In the present version of the model, skeletal
caesium is divided into four specific pools that appear to contain nearly all of theskeletal content (Williams and Leggett, 1987): red marrow, cartilage, trabecular bone
surface, and cortical bone surface.
2. A simplistic representation of the gastrointestinal (GI) tract used in the original model
to describe exchange of caesium between systemic and GI pools is replaced here by
the GI portion of the HATM.
(289) The structure of the model as applied in this report is shown in Figure 5-1. Baseline
parameter values are listed in Table 6-3. Most of the parameter values were taken from Table
2 of Leggett et al. (2003), which provides baseline values for a reference adult male for thecase of a well-mixed plasma pool. Modification or addition of some parameter values was
96DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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3800

3801
3802
3803
3804
3805
3806
3807
3808
3809
3810
3811
3812
3813
3814
3815
3816
3817
3818
3819
3820
3821

required due to the structural differences between the present and original versions of themodel indicated above. The methods of derivation of the values in Table 6-3 are summarized
below.

Figure 6-1. Structure of the model for systemic caesium and its exchange with caesiumin the alimentary tract. Abbreviations: Trab = trabecular, Cort = cortical, surf = surface,
UB = urinary bladder, cont = contents, RBC = red blood cells, St = stomach, SI = small
intestine, RC = right colon, LC = left colon, RS = rectosigmoid colon.
(290) The derivation of most parameter values involves reference values for cardiac output
and the percentage of cardiac output received by individual tissues. The assumed cardiac
output in a resting adult male is 1766 plasma volumes d-1. The assumed distribution ofcardiac output is given in Table 6-4.
(291) Movement of caesium is depicted as a system of first-order processes. The transfer
coefficient from plasma into a tissue T is estimated as the product of the plasma flow rate tothat tissue (1766 plasma volumes per day multiplied by the fraction of cardiac output received
by the tissue) and a tissue-specific extraction fraction, ET. The extraction fraction for a tissue
is defined as the fraction of caesium atoms extracted by that tissue during passage of caesium
from arterial to venous plasma.
(292) Data on tissue-specific extraction fractions for caesium (Cs) and its physiologicalanalogues potassium (K) and rubidium (Rb) were reviewed by Leggett and Williams (1986,
1988) and Leggett et al. (2003). In general, tissue extraction from plasma decreases in theorder K ≥ Rb > Cs. For example, extraction by the myocardium in dogs was estimated as

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3839

0.71 (range, 0.64-0.80) for potassium, 0.65 (0.58-0.76) for rubidium, and 0.22 (0.09-0.30) for
caesium (Love et al., 1968; Poe, 1972). More information on extraction fractions was foundfor potassium and rubidium than for caesium. Data for potassium and rubidium wereextrapolated to caesium by applying modifying factors as indicated by data on discrimination
between these elements by tissues (Leggett et al., 2003). Initial selections of extraction
fractions were modified in some cases after testing the model against reported caesium
distributions in the early minutes or hours after administration to laboratory animals (Carr,
1966; Love et al., 1968; Yano et al., 1970; Stather, 1970; Poe, 1972; Moskalev, 1972; Krulik
et al., 1980; Gregus and Klaasen, 1986; Nishiyama et al., 1975) or human subjects (Rosoff etal., 1963; Nishiyama et al., 1975). For example, an initially selected extraction fraction of
0.003 for brain was reduced to 0.002 for improved agreement with observations of the timedependent increase of the caesium content of the brain following acute intake. The final
selections of extraction fractions for caesium are as follows: 0.2 for kidneys, walls of thegastrointestinal tract, and heart wall; 0.05 for liver and skin; 0.002 for brain; and 0.1 for allother tissues.
Table 6-3. Transfer coefficients for the model for systemic caesium

From
PlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaRed blood cells
MuscleLiver
Liver
KidneysTo
Red blood cells
Skeletal muscle
Liver
Kidneys
SpleenPancreas
Skin
Adipose tissue
Brain
Heart wall
Lung tissue
Red marrow
Cartilage
Trabecular bone surface
Cortical bone surface
Stomach wall
Stomach content
Small intestine wall
Small intestine content
Right colon wall
Right colon content
Left colon wall
Rectosigmoid colon wall
Other 1Other 2
PlasmaPlasmaPlasmaSmall intestine content
Urinary bladder content

98

Transfer coefficient
(d-1)
1.8
30.0
19.5
67.1
5.30
1.77
4.42
8.83
0.424
14.1
4.42
5.3
3.0
1.59
1.06
3.53
4.52
35.3
1.05
5.65
0.02
5.65
2.83
9.71
0.00353
0.257
0.0751
2.14
0.113
1.68

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
Kidneys
SpleenSpleenPancreas
Pancreas
Skin
Skin
Adipose tissue
Brain
Heart wall
Lung tissue
Red marrow
Cartilage
Trabecular bone surface
Cortical bone surface
Stomach wall
Stomach wall
Stomach wall
Small intestine wall
Small intestine wall
Small intestine wall
Right colon wall
Right colon wall
Right colon wall
Left colon wall
Left colon wall
Left colon wall
Rectosigmoid colon wall
Rectosigmoid colon wall
Rectosigmoid colon wall
Other 1Other 2
3840
3841
3842
3843
3844
3845
3846
3847
3848
3849

PlasmaPlasmaLiver
PlasmaLiver
PlasmaExcreta
PlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaLiver
Stomach content
PlasmaLiver
Small intestine content
PlasmaLiver
Right colon content
PlasmaLiver
Left colon content
PlasmaLiver
Rectosigmoid colon content
PlasmaPlasma

31.9
5.03
0.265
1.68
0.08830.867
0.01591.77
0.0848
8.07
1.47
0.706
0.2
0.212
0.212
4.16
0.219
0.21
9.87
0.519
0.21
6.86
0.361
0.21
6.86
0.361
0.21
6.86
0.361
0.21
0.762
0.00141(293) The transfer coefficient from a tissue T to plasma is based on the relative contents of
caesium in plasma and T at equilibrium (Table 6-4), as estimated from collected studies ofstable and radioactive caesium in living human subjects and cadavers (Williams and Leggett,
1987; Leggett et al., 2003). If T exchanges caesium only with plasma, the transfer coefficientR2 from T to plasma is determined as R2 = R1 x P/A, where A and P are the fractions of totalbody caesium in the tissue and plasma at equilibrium and R1 is the transfer coefficient fromplasma to T.

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3853

Table 6-4. Reference distribution of cardiac output and steady-state distribution of stablecaesium in an adult malea

Compartment
PlasmaRed blood cells (RBC)
Skeletal muscle
Liver
Kidneys
SpleenPancreas
Stomach wall
Small intestine wall
Right colon wall
Left colon wall
Rectosigmoid colon wall
GI contentsb
Red marrow
Trabecular bonec
Cortical bonec
Cartilage
Skin
Heart wall
Lung tissue
Brain
Adipose tissue
OtherdTotals
a

b
c
d

3854
3855
3856
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3858
3859
3860
3861
3862
3863
3864

Caesium content at equilibrium(% of total body)
0.2
1.4
80
2.0
0.4
0.2
0.2
0.154
0.667
0.152
0.152
0.076
0.4
1.5
1.5
1.0
3.0
1.0
0.35
0.6
1.0
1.0
3.05
100

Blood flow rate(% of cardiac output)--17
6.5 (arterial) + 19 (portal)
19
3.0
1.0
1.0
10
1.6
1.6
0.8
-3.0
0.9
0.6
-5.0
4.0
2.5
12
5.0
5.5
100

Based on estimates of Leggett et al. (2003). Values for GI tissue compartments based on estimate for total
GI tissue and mass fractions of individual tissues. Division of skeletal caesium based on a review by
Williams and Leggett (1987).
Sum of contents of stomach, small intestine, right colon, left colon, and rectosigmoid colon.
In the model, all caesium in bone is assumed to reside on bone surface.
In the model, Other is divided into compartments Other 1 and Other 2 with fast and slow exchange withplasma, respectively. Other 1 receives 5.498% of cardiac output and contains 2.55% of total-body caesium
at equilibrium. Other 2 receives 0.002% of cardiac output and contains 0.5% of total-body caesium atequilibrium.

(294) The use of extraction fractions and the equilibrium distribution for caesium to derivetransfer coefficients between plasma and tissues is illustrated for skeletal muscle. The
transfer coefficient from plasma to skeletal muscle is estimated as 0.1 x 0.17 x 1766 d-1 =30.022 d-1, where 0.1 is the estimated extraction fraction for skeletal muscle, 0.17 is thereference fraction of cardiac output going to skeletal muscle, and 1766 d-1 is the reference
cardiac output in plasma volumes per day. The transfer coefficient from skeletal muscle toplasma is 0.002 x 30.022 d-1 / 0.8 = 0.0751 d-1, where 0.002 and 0.8 are, respectively,
fractions of total-body caesium in plasma and skeletal muscle at equilibrium. Derived
parameter values are rounded to three significant digits in Table 6-3.
(295) The concept of an extraction fraction does not apply to red blood cells (RBC). The

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transfer coefficients between plasma and RBC are derived from observed transfer rates forpotassium and comparative data on potassium and caesium. The transfer coefficient forpotassium from plasma to RBC is estimated from data from several experimental studies as 6
d-1 (Leggett and Williams, 1986, 1988). The rate of transfer of caesium into RBC is roughly
0.3 times that of potassium in humans, rabbits, and rats (Love and Burch, 1953; Forth et al,
1963; Gyorgyi and Kanyar, 1973) and thus is estimated as 0.3 x 6 d-1 = 1.8 d-1. The transfer
coefficient from RBC to plasma can be determined from the caesium inflow rate (1.8 d-1) andthe equilibrium fractions of caesium in plasma and RBC, respectively. Based on thereference steady-state content of RBC (as a fraction of total-body caesium; see Table 6-4) thetransfer coefficient from RBC to plasma is 1.8 d-1 x 0.002 / 0.014 = 0.257 d-1.
(296) The concept of an extraction fraction also does not apply to cartilage, which contains
no blood vessels but receives nutrients via a permeable matrix in contact with extravascular
fluids. The simplifying assumption is made here that cartilage receives caesium directly fromplasma and returns caesium to plasma. Transfer coefficients describing exchange between
plasma and cartilage are set to depict rapid uptake and subsequently elevated concentration ofradiocaesium in cartilage as observed in different animal species (Nelson et al., 1961; Ekman,
1961; Furchner et al., 1964) and to yield a cartilage content of 3% of total-body caesium atequilibrium (Williams and Leggett, 1987).
(297) For a compartment T that receives caesium from plasma but loses caesium tomultiple compartments, the total outflow rate R from T is derived as illustrated above forskeletal muscle, and additional information is used to divide R into transfer coefficients
representing different paths of movement. For example, the derived rate of loss R from skinis divided into transfer coefficients R1 and R2 representing the rate of loss from skin to plasma
and the rate of loss from skin to sweat, respectively. The value for R2 is set for consistency
with data of Yamagata et al. (1966) on the appearance of activity in sweat after ingestion of132
Cs by a human subject, and R1 is determined as R – R2. As a second example, thecompartment representing the stomach wall is assumed to return caesium to plasma via theportal vein and to lose caesium to the stomach contents due to cell sloughing. The total rate ofloss R (4.59 d-1) from the stomach wall to all destinations is derived as illustrated earlier forskeletal muscle. The transfer coefficient from the stomach wall to the stomach contents
representing cell sloughing is set at 0.21 d-1, an estimated average cell sloughing rate from GI
tract tissues to GI contents (Leggett et al., 2003). The rate of loss of caesium from thestomach wall via the portal vein is calculated as the total removal rate from stomach wall
minus the rate of cell sloughing: 4.59 d-1 – 0.21 d-1 = 4.38 d-1. Outflow from the stomachwall via the portal vein is divided between the plasma and liver compartments on the basis of
the extraction fraction for liver (0.05). That is, the transfer coefficient from the stomach wall
to the liver is 0.05 x 4.38 d-1 = 0.219 d-1, and the transfer coefficient from the stomach wall toplasma is 0.95 x 4.38 d-1 = 4.16 d-1.
(298) Some of the transfer coefficients are based on a combination of basic physiological
data and empirical data for caesium. For example, the rate of transfer of caesium into thegastrointestinal tract in liver bile is estimated as 5% of total outflow from the liver based ondata on the rate of bile flow in man and observed concentration ratios for caesium in liver andbile in different animal species. A total outflow rate from the liver of 2.25 d-1 is based on thederived transfer coefficient from plasma to liver of 19.5 d-1 and the assumption that the liver
contains 2% of total-body caesium at equilibrium. The transfer coefficient from liver to bile iscalculated as 0.05 x 2.25 d-1 = 0.113 d-1.
(299) Urinary excretion of caesium is depicted as transfer from plasma to a well-mixed
kidney compartment and division of outflow from that compartment to plasma and the101

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contents of the urinary bladder. Transfer from plasma to kidneys is represented as aneffective extraction fraction times the blood flow rate to kidneys, where the effective
extraction fraction includes atoms temporarily retained in the tubules after filtration at theglomerulus as well as atoms entering kidney tissue directly from blood plasma. The divisionof kidney outflow between plasma and urinary bladder contents is set for consistency withshort-term urinary excretion data for healthy adult males (Lloyd et al., 1972, 1973). It is
assumed that the renal deposit represents the only source of urinary caesium. That is, it isassumed that none of the urinary caesium arises from filtered or secreted atoms that pass tothe urinary bladder without being retained in kidney tissue.
(300) Endogenous faecal excretion is assumed to arise from transfer of caesium into thecontents of the alimentary tract in saliva, gastric juices, pancreatic secretions, liver bile, andother secretions. It is assumed that 99% of the secreted activity that reaches the small
intestine is reabsorbed to blood and that absorption occurs only in the small intestine.
(301) The model depicts a small component of very long-term retention observed inhuman subjects involved in the accident in Goiania, Brazil (Melo et al., 1997, 1998) and inexperimental studies on rats that received 137Cs by intraperitoneal injection (Thomas andThomas, 1968). In eight adult human subjects involved in the Goiania accident, this small
component of retention had an estimated half-time on the order of 500 d and represented an
estimated 0.01-0.25% of uptake to blood, with estimates falling between 0.04% and 0.07%
for five of the eight subjects. In rats, this component represented less than 0.01% of injected137
Cs and had a half-time of 150-200 d. The physiological basis for this retention component
is not known. It is represented in the model as a compartment called “Other 2” that isassumed to receive 0.002% of cardiac output and to contain 0.5% of total-body caesium atequilibrium. This long-term component of retention does not represent an important
contribution to dose per unit intake of radiocesium but can be important for interpretation of
bioassay data collected at times remote from exposure.
(302) As is the case for the original model, the present version of the model can be used tosimulate the effect of binding of caesium to Prussian Blue (PB) or other unabsorbed material
in the gut. The simulation is carried out by changing the relative fractions of caesium assumed
to move from the small intestine contents to blood and to the right colon contents. If it isassumed that all caesium entering the small intestine is carried by PB to the right colon
contents and is eventually excreted in faeces, the long-term retention half-time for the adultmale decreases by about 60%. Melo et al. (1998) found that oral administration of PB
reduced the long-term retention half-time by an average of 69% (range, 36-83%) in 11 adultmale subjects. Ruwei et al. (1985) found an average reduction in the half-time of about 50%
in five subjects. Madshus et al. (1966) found an average reduction of 64% in two subjects.
6.2.3.3. Treatment of radioactive progeny(303) Four caesium isotopes addressed in this report have radioactive progeny that may
contribute significantly to dose estimates for the parent, depending to some extent on theassumed behavior of the progeny: 125Cs, 127Cs, 134mCs, and 137Cs. Cesium-134m (T1/2 = 2.9 h)
decays to 134Cs (T1/2 = 2.06 y), which presumably behaves as if entering its site of production
as a parent radionuclide. The other three cesium isotopes decay to radionuclides that are
expected to migrate to some extent from the parent radionuclide.
(304) Cesium-125 (T1/2 = 45 m) decays to the noble gas 125Xe (T1/2 = 16.9 h), which
decays to 125I (T1/2 = 59.4 d). Xenon-125 produced by decay of 125Cs in bone is assumed totransfer to blood at the rate 100 d-1 if produced in a bone surface compartment and 0.36 d-1 if
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produced in a bone volume compartment. These rates are taken from the model for radon
introduced in ICRP Publication 67 (1993) and applied in this report to radon produced inbone surface and non-exchangeable bone volume, respectively, by decay of a radium isotope.
Xenon produced in a soft-tissue compartment is assumed to transfer to blood with a half-timeof 20 min. Xenon entering blood is assumed to be removed from the body (exhaled) at therate 1000 d-1, corresponding to a half-time of 1 min. Partial recycling of xenon to tissues via
arterial blood is not depicted explicitly in this model for xenon as a daughter radionuclide but
is considered in the assignment of the half-times in tissues. The model is intended to yield aconservative average residence time of xenon atoms in the body after their production insystemic pools.
(305) Iodine-125 produced by serial decay of 125Cs and 125Xe is assumed to follow thecharacteristic model for iodine (the model applied in this report to iodine as a parent
radionuclide) from its time of production in a compartment of the caesium model that is
identifiable with a compartment of the characteristic model for iodine. For example, thecompartments of the caesium model representing liver and kidneys are assumed to correspondto the compartments for liver iodide and kidney iodide in the characteristic model for iodine.
When produced in a compartment that is not identifiable with a compartment in thecharacteristic model for iodine, 125I generally is assumed to transfer rapidly to blood (at therate 330 d-1, the highest transfer rate to blood in the iodine model) and then to follow thecharacteristic model for iodine. An exception is that 125I produced in red blood cells is
assumed to transfer to the iodide blood pool in the iodine model at the rate 1000 d-1.
(306) Caesium-127 (T1/2 = 6.25 h) decays to the noble gas 127Xe (T1/2 = 36.4 d). In thiscase inclusion of decays of the progeny based on the xenon model described above has anegligible effect on dose estimates for the parent due to the relatively long half-life of thexenon isotope.
(307) Cesium-137 (T1/2 = 30.2 y) decays to 137mBa (T1/2 = 2.55 min). Wasserman et al.
(1959) demonstrated considerable dissociation of 137mBa from 137Cs in rats at 4-7 d after
intraperitoneal administration of 137Cs/137mBa, despite the short half-life of 137mBa. Barium137m was found to exceed equilibrium proportions in bone, blood, and plasma by factors of
3.3, 3.9, and 14, respectively. Some soft tissues were moderately deficient in 137mBa, whileothers showed little or no deviation from equilibrium. The authors concluded neverthelessthat soft tissues likely were the main source of the excess 137mBa in plasma and that red blood
cells probably also contributed to the excess. Skeletal muscle was not sampled but seems
likely to have been a major contributor to the excess 137mBa in plasma and bone as itpresumably contained the preponderance of systemic 137Cs after 4-7 d.
(308) The model applied in this report to barium as a parent radionuclide was modified in
the following ways for application to 137mBa produced in systemic pools by decay of 137Cs:(1) compartments and pathways not relevant to the short-term behavior of systemic barium
were eliminated; and (2) the rate of exchange of barium between plasma and a rapid-turnoversoft-tissue compartment as well as the rates of transfer of barium to tissues and excretion
pathways were increased to provide an improved fit to blood clearance data for humansubjects immediately following intravenous injection of 133Ba (Newton et al., 1991). Kinetic
studies with radioisotopes of barium and other alkaline earth elements indicate that theseelements initially leave plasma with a half-time of a few minutes and equilibrate rapidly withan extravascular pool about three times the size of the plasma pool (Newton et al., 1991;
Leggett, 1992). Studies of the short-term behavior of 133mBa in human subjects indicate thatthe important repositories for barium during the early minutes after intravenous
administration are bone and colon (Korsunskii et al., 1986). The following systemic model
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for 137mBa produced by decay of 137Cs is based on these considerations and the findings ofWasserman et al. (1959) regarding the dissociation of 137mBa from 137Cs in rats. Barium
produced in skeletal muscle and red blood cells transfers to plasma at the rate 1000 d-1, thedefault value for extremely rapid transfer between systemic compartments. Barium produced
in all other soft tissue compartments transfers to plasma at the rate 200 d-1 (half-time of 5min), chosen to yield at most a moderate deficiency of 137mBa in these tissues compared withequilibrium values. Barium produced in bone decays at its site of production. Bariumtransfers from plasma to: trabecular bone surface at the rate 19.4 d-1, cortical bone surface at
15.6 d-1, right colon contents at 40.3 d-1, urinary bladder contents at 4.48 d-1, and acompartment representing all soft tissues at 184 d-1. The transfer coefficient from the soft
tissue compartment back to plasma is 61.4 d-1. Barium entering the urinary bladder or rightcolon contents follows the generic excretion models. The transfer coefficients from plasma tobone surface compartments and excretion pathways are two times the corresponding values
given in the model for barium as a parent. The rates of transfer between plasma and the soft
tissue compartment are set to fit the early plasma clearance data of Newton et al. (1991) for
human subjects, with the constraint that the transfer coefficient from soft tissues to plasma is
one-third the coefficient from plasma to soft tissues. This constraint implies that the content
of the soft-tissue compartment is three times that of plasma at equilibrium. The model
predicts that the plasma content of 137mBa at 4-7 d after injection of 137Cs to blood is 13-16
times the equilibrium value, which is consistent with findings of Wasserman et al. (1959) forrats. The bone content of 137mBa at 4-7 d is predicted to be roughly 2 times the equilibrium
value compared with the ratio 3.3 determined by Wasserman and coworkers. The high rate of
migration of 137mBa from its sites of production to bone indicated by the findings for rats
could not be reproduced while remaining consistent with reported biokinetic data, e.g. blood
clearance data, for barium in human subjects.
6.2.3.4. Differences with gender(309) The long-term biological half-time of caesium in the total body, representing roughly
90% of absorbed caesium, typically is about one-fourth (15-35%) lower in women than in
men and about one-third lower in pregnant than in non-pregnant women. During lactation
there is substantial transfer of caesium from blood to the mammary glands to milk (ICRP,
2004).
6.3.

Individual monitoring(310) 134Cs internal exposures may be detected using urinalysis or in vivo Whole Body
counting.

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4047

Isotope
134

Cs
Cs

134

134

Cs

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MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
1 Bq/L
γ-ray spectrometry
Whole
Body γ-ray spectrometry, 20-40 Bq
Counting
in vivo(shielded room)
Lung Monitoring
γ-ray spectrometry, 9 Bq*
in vivo

Achievabledetection limit
0.04 Bq/L
11 Bq∗ Lung monitoring of 134Cs is not generally used in routine monitoring of workers. Monte Carlo program
Visual Monte Carlo was used to simulate the photon emission, to calculate the calibration factor for thegeometry and radionuclide, and to calculate the minimum detectable activity (MDA) in the lung. (Hunt et al,2012)(311) 137Cs internal exposures are detected by gamma spectroscopy using the 0.661 MeV
gamma ray from its daughter 137mBa (T1/2 =2.5 min), which is produced in approximately
94.4 % of decays of 137Cs and exists in secular equilibrium with 137Cs in the body. Gamma
spectroscopy is used for in vivo measurements and for excreta analysis.
Isotope

4058
4059
4060
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4062
4063
4064
4065
4066
4067
4068
4069
4070
4071
4072
4073
4074
4075
4076
4077

Monitoring
Technique

137

Cs

137

Cs

137

Cs

Monitoring
Technique

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
γ-ray spectrometry 1-5 Bq/L
from 137mBa
Lung monitoring
γ-ray spectrometry 11 Bq*
from137mBa
Whole
Body γ-ray spectrometry 25-60 Bq
Counting
from137mBa(shielded room)

Achievabledetection limit
0.1 Bq/L

16 Bq∗ Lung monitoring of 137Cs is not generally used in routine monitoring of workers. Monte Carlo program
Visual Monte Carlo was used to simulate the photon emission, to calculate the calibration factor for thegeometry and radionuclide, and to calculate the minimum detectable activity (MDA) in the lung. (Hunt et al,2012)

References
Al Rayyes, A.H., Ronneau, C., Stone, W.E., Genet, M.J., Ladière, J., Cara. J., 1993. Radiocaesium in
Hot particles: solubility vs chemical speciation. J. Environ. Radioact., 21, 143-151.
Andrieu, L., Fatome, M., 1979. Évolution lontaine inattenfue d’une contamination interne.
Radioprotection 14(3), 135-143.
Boecker, B. B., Cuddihy, R.G., Hahn, F F., McClellan, R.O., 1974. A seven year study of thepulmonary retention and clearance of 137Cs inhaled in fused aluminosilicate particles by the
beagle dog. Inhalation Toxicology Research Institute Annual Report 1973–1974, LF–49, pp.
48–52. Lovelace Biomedical and Research Foundation, Albuquerque, New Mexico.
Available from National Technical Information Service, Springfield, Virginia.
Boecker, B.B., 1969a. The metabolism of 137Cs inhaled as 137CsCl by the beagle dog. Proc. Soc. Exp.
Biol. Med. 30, 966-971.
Boecker, B.B., 1969b. Comparison of 137Cs metabolism in the beagle dog following inhalation andintravenous injection. Health Phys., 16, 785–788

105

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
4078
4079
4080
4081
4082
4083
4084
4085
4086
4087
4088
4089
4090
4091
4092
4093
4094
4095
4096
4097
4098
4099
4100
4101
4102
4103
4104
4105
4106
4107
4108
4109
4110
4111
4112
4113
4114
4115
4116
4117
4118
4119
4120
4121
4122
4123
4124
4125
4126
4127
4128
4129

Carr, E.A., 1966. Pharmacology of radioactive caesium salts. In: Andrews GA, Kniseley RM, Wagner
HN, editors. Radioactive Pharmaceuticals, Proceedings of a symposium held at Oak Ridge
Associated Universities, Nov 1-4, 1965, USAEC; CONF-651111, pp. 619-634.
Cecchi, X., Wolff, D., Alvarez, O., Latorre, R., 1987. Mechanisms of Cs+ blockade in a Ca2+activated K+ channel from smooth muscle. Biophys. J., 52, 707-716
Cryer, M.A., Baverstock, K.F., 1972. Biological half-time of 137Cs in man. Health Phys., 23, 394-395.
Cuddihy, R.G., Finch, G.L., Newton, G.J., Hahn, F.F., Mewhinney, J.A., Rothenberg, S.J., Powers,
D.A., 1989. Characteristics of radioactive particles released from the Chernobyl nuclear
reactor. Environ. Sci. Technol., 23, 89–95.
Cuddihy, R.G., Ozog, J.A., 1973. Nasal absorption of CsCl, SrCl2, BaCl2, and CeCl3 in Syrian
Hamsters. Health Phys., 25, 219–224.
Dua, S.K., Maniyan, C.G., Kotrappa, P., 1987. Inhalation exposures during operations in spent fuelbays. Radiat. Prot. Dosim., 19, 165–172.
Edwards, C., 1982. The selectivity of ion channels in nerve and muscle. Neuroscience 7, 1335-1366.
Ekman, L., 1961, Distribution and excretion of radio-cesium in goats, pigs and hens. Acta Vet. Scand.
2 (Suppl. 4):1-83.
Forth, W., Oberhausen, E., Pfleger, K., Weske, G., 1963. Beitrag zur Kloumarung der Ursachen derAnreicherung von Caesium-137 im Organismus. Experientia, 19, 25-26.
Froning, M., Kozielewski, T., Schlager, M., Hill, P., 2004. A case study of the long-term retention of137
Cs after inhalation of high temperature reactor fuel element ash, Radiat. Prot. Dosim.,
111(1), 55-58.
Furchner, J. E.; Trafton, G. A.; Richmond, C. R. , 1964. Distribution of cesium-137 after chronic
exposure in dogs and mice. Proc. Soc. Exp. Biol. Med. 116:375-378.
Gregus, Z., Klaassen, C.D., 1986. Disposition of metals in rats: A comparative study of fecal, urinary,and biliary excretion and tissue distribution of eighteen metals. Toxicol Appl. Pharmacol., 85,
24-38.
Gyorgyi, S., Kanyar, B., 1973. Comparison of Cs-137 and K-42 transport of rat erythrocytes bymeans of a tracer kinetic model. In: Bujdoso E. Proceedings of the IRPA second European
congress on radiation protection, pp. 263-268.
Hesp, R., 1964. The retention and excretion of caesium-137 by two male subjects. In Assessment ofRadioactivity in Man. Vol. II. IAEA, Vienna, pp. 61-74.
Hodgkin, A.L., 1947. The effect of potassium on the surface membrane of an isolated axon. J.
Physiol., 106, 319-340.
Hölgye, Z., Malý, M., 2002. A case of repeated accidental inhalation contamination of a male subject
with 137Cs. Health Phys., 82(4), 517-520.
ICRP, 1979. Limits for intakes of radionuclides by workers. ICRP Publication 30, Part 1. Oxford:
Pergamon Press.
ICRP, 1989. Age-dependent Doses to Members of the Public from Intake of Radionuclides. Part 1.
ICRP Publication 56. Ann. ICRP 20(2).
ICRP, 1993. Age-dependent Doses to Members of the Public from Intake of Radionuclides. Part
2.Ingestion dose coefficients. ICRP Publication 67. Ann. ICRP 23(3-4).
ICRP, 1994. Dose coefficients for intake of radionuclides by workers. ICRP Publication 68, Ann.
ICRP 24 (4).
ICRP, 2002a. Supporting Guidance 3. Guide for the Practical Application of the ICRP Human
Respiratory Tract Model. Ann. ICRP 32(1-2).
ICRP, 2002b. Basic anatomical and physiological data for use in radiological protection: reference
values. ICRP Publication 89, Ann. ICRP 32 (3-4).
ICRP, 2004. Doses to infants from ingestion of radionuclides in monthers' milk. ICRP Publication 95.
Ann ICRP 34 (3-4).
Korsunskii, V.N., Tarasov, N.F., Naumenko, A.Z., 1981. Clinical evaluation of Ba-133m as an
osteotropic agent. ORNL/TR-86/30 (7 pgs); Translated from the Russian UDC 616.71-006073.916, Meditsinskaya Radiologiya No. 10, pp. 45-48.

106

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
4130
4131
4132
4133
4134
4135
4136
4137
4138
4139
4140
4141
4142
4143
4144
4145
4146
4147
4148
4149
4150
4151
4152
4153
4154
4155
4156
4157
4158
4159
4160
4161
4162
4163
4164
4165
4166
4167
4168
4169
4170
4171
4172
4173
4174
4175
4176
4177
4178
4179
4180

Kotrappa, P., Bhat, I.S., Vashi, V.D., 1977. Particle size and solubility characteristics of aerosols in
Pu processing areas and BWR type power reactors. IN Proceedings of the FourthInternational Congress of the International Radiation Protection Association (IRPA) Paris
Vol. 3, pp. 771–774.
Krulik, R., Farska, I., Prokes, J., Tykva, R., 1980. Distribution of caesium in the organism and its
effect on the nucleotide metabolism enzymes. Int. Pharmacopsychiat. 15, 157-165.
Kutkov, V.A., 1998. Application of human respiratory tract models for reconstruction of the size ofaerosol particles through the investigation of radionuclides behaviour in the human body.
Radiat. Prot. Dosim., 79, 265–268.
Kutkov, V.A., 2000. Results of in vivo monitoring of the witnesses of the Chernobyl accident.
Radiat. Prot. Dosim. 89, 193-197.
Kutkov, V.A., Komaritskaya, O.I., 1996. In vitro solubility of Chernobyl nuclear fuel aerosol withrespect to collective behaviour of its radionuclides. In : Proc. IRPA 9, Vienna, 2, 445-447.
Latorre, R., Miller, C., 1983. Conduction and selectivity in potassium channels. J Membr. Biol.
71:11-30.
Leggett, R. W., 1992. A generic age-specific biokinetic model for calcium-like elements. Radiat. Prot.
Dosim., 41,183-198.
Leggett, R.W., 1986. Predicting the retention of caesium in individuals. Health Phys., 50, 747-759.
Leggett, R.W., Bouville, A., Eckerman, K.F., 1998. Reliability of the ICRP’s systemic biokinetic
models. Radiat. Prot. Dosim., 79, 335-342.
Leggett, R.W., Williams, L.R., 1986. A model for the kinetics of potassium in healthy humans. Phys.
Med. Biol., 31, 23-42.
Leggett, R.W., Williams, L.R., 1988. A biokinetic model for rubidium in humans. Health Phys., 55,
685-702.
Leggett, R.W., Williams, L.R., 1995. A proposed blood circulation model for Reference Man. HealthPhys., 69, 187-201.
Leggett, R. W.; Williams, L. R.; Eckerman, K. F. (1999). A blood circulation model for referenceman. In: Proceedings of the 6th Annual Radiopharmaceutical Dosimetry Symposium; A. T.
S.-Stelson, M. G. Stabin, and R. B. Sparks, eds. (Oak Ridge, TN: Oak Ridge Institute for
Science and Education); pp. 487-499.
Leggett, R.W., Williams, L.R., Melo, D.R., Lipsztein, J.L., 2003. A physiologically based biokinetic
model for caesium in the human body. The Science of the Total Environment 317, 235-255.
LeRoy, G.V., Rust, J.H., Hasterlik, R.J., 1966. The Consequences of Ingestion by Man of Real and
Simulated Fallout. Health Phys., 12, 449-473.
Lie, R., 1964. Deposition and retention of 137Cs in the rat following inhalation of the chloride and thenitrate. Health Phys., 10, 1071–1076.
Lloyd, R.D., Mays, C.W., McFarland ,S.S., Zundel, W.S., Tyler, F.H., 1972. Rb-86 and Cs-137
metabolism in persons affected by muscle disease. In: University of Utah Report
COO-119-247, University of Utah College of Medicine. Salt Lake City, UT, pp. 1-72.
Lloyd, R.D., Mays, C.W., McFarland, S.S., Zundel, W.S., Tyler, F.H., 1973. Metabolism of Rb-83
and Cs-137 in persons with muscle disease. Radiat Res., 54, 463-478.
Lloyd, R.D., Zundel, W.S., Mays, C.W., Wagner, W.W., Pendelton, R.C., 1966. Enhanced Cs-137
elimination in pregnant and dystrophic humans. Radiat. Res., 27, 548.
Love, W.D., Burch, G.E., 1953. A comparison of K-42, Rb-86, and Cs-134 as tracers of potassium inthe study of cation metabolism of human erythrocytes in vitro. J. Lab. Clin. Med., 41,351-362.
Love, W.D., Ishihara, Y., Lyon, L.D., Smith, R.O., 1968. Differences in the relationships between
coronary blood flow and myocardial clearance of isotopes of potassium, rubidium, andcaesium. American Heart J., 76, 353-355.
Madshus, K., Stromme, A., Bohne, F., Nigrovic, V., 1966. Diminution of radiocaesium body-burdenin dogs and human beings by Prussian Blue. Int. J. Radiat. Biol., 10, 519-520.

107

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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4195
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4197
4198
4199
4200
4201
4202
4203
4204
4205
4206
4207
4208
4209
4210
4211
4212
4213
4214
4215
4216
4217
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4219
4220
4221
4222
4223
4224
4225
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4227
4228
4229
4230
4231

McKay, W.A., Memmott, S.D., 1991. An investigation of the availability of 137Cs and 239 + 240Pu
for gut absorption in winkles following cooking and in vitro simulated gastro-intestinal
digestion. Food Addit. Contam., 8, 781-786.
Melo, D.R., Lipsztein, J.L., Oliveira, C.A., Lundgren, D.L., Muggenburg, B.A., Guilmette, R.A.,
1997. A biokinetic model for 137Cs. Health Phys., 73, 320-332.
Melo, D.R., Lipsztein, J.L., Oliveira, C.A., Lundgren, D.L., Muggenburg, B.A., Guilmette, R.A.,
1998. Prussian Blue decorporation of 137Cs in humans and beagle dogs. Radiat. Prot. Dosim.,
79, 473-476.
Miller, C.E., 1964. Retention and distribution of 137Cs after accidental inhalation. Health Phys. 10,
1065–1070.
Mirell, S. G., Blahd, W.H., 1989. Biological retention of fission products from the Chernobyl plume.
Health Phys., 57, 649–652.
Morrow,P.E., Gibb,F.R., Davies, H., Fisher, M., 1968. Dust removal from the lung parenchyma: aninvestigation of clearance stimulants. Toxicol. Appl. Pharmacol., 12, 372-396.
Moskalev,Yu., I. 1972. Distribution and acceleration of radioisotope excretion. Distribution of
caesium-137 in the animal organism. AEC-TR-7512, pp. 4-19.
Naversten, Y., Liden, K., 1964. Half-life studies of radiocaesium in humans. In: Assessment ofradioactivity in man, Vol II (Vienna: IAEA), pp. 79-87.
Nelson, A.; Ullberg, S.; Kristoffersson, H.; Ronnback, C., 1961. Distribution of radiocesium in mice.
Acta Radiol. 55:374-384.
Newton, D., Harrison, G.E., Kang, C., Warner, A. J., 1991. Metabolism of injected barium in six
healthy men. Health Phys., 61, 191-201.
Nishiyama, H., Sodd, V.J., Schreiber, T.J., Loudon, R.G., Saenger, E.L., 1975. Imaging of
pulmonary tumors with 129Cs. In: Subramanian, G., Rhodes, B.A., Cooper, J.F., Sodd, V.J.,(Eds.), Radiopharmaceuticals, New York, NY, The Society of Nuclear Medicine, pp. 482490.
Poe, N.D., 1972. Comparative myocardial uptake and clearance characteristics of potassium andcaesium. J. Nucl. Med., 13:557-560.
Raghavendran, K., Satbhai, P.D., Abhyankar, B., Unnikrishnan, K., Somasundaram, S., 1978. Longterm retention studies of 131I, 137Cs and 60Co in Indian workers, Health Phys., 34, 185-188.
Rosoff, B., Cohn, S.H., Spencer, H.I., 1963. Caesium-137 metabolism in man, Radiat. Res., 19,643-654.
Rundo, J., 1964. The metabolism of biologically important radionuclides. VI. A survey of themetabolism of caesium in man. Brit. J. Radiol., 37, 108-114.
Rundo, J., 1965. A case of accidental inhalation of irradiated uranium. Brit. J. Radiol., 38, 39–50.
Rundo, J., Mason, J., Newton, D., Taylor, B., 1963. Biological half-life of caesium in man in acuteand chronic exposure. Nature, Lond., 200, 188-189.
Ruwei, M.A., Yueru, J., Songling, W., 1985. Study of 137Cs metabolism in humans. In: Assessment ofradioactive contamination in man (Vienna: IAEA), IAEA-SM-276/59, pp. 499-506.
Sjodin, R.A., Beauge, L.A., 1967. The ion selectivity and concentration dependence of cation
coupled active sodium transport in squid giant axons. Curr. Mod. Biol., 1, 105-115.
Snipes, M.B., Boecker, B.B., McClellan, R.O., 1983. Retention of monodisperse or polydisperse
aluminosilicate particles inhaled by dogs, rats, and mice. Toxicol. Appl. Pharmacol., 69, 345–
362.
Snipes, M.B., McClellan, R.O., 1986. Model for deposition and long-term disposition of 134Cslabeled fused aluminosilicate particles inhaled by guinea pigs. Inhalation Toxicology
Research Institute Annual Report 1985–1986, LMF–115, pp. 91–95. Lovelace Biomedical &Environmental Research Institute, Albuquerque, New Mexico. Available from National
Technical Information Service, Springfield, Virginia.
Stara, J.F., 1965. Tissue distribution and excretion of caesium-137 in the guinea pig afteradministration by three different routes. Health Phys., 11, 1195–1202.

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4260
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4263
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Stather, J.W., 1970. An analysis of the whole-body retention of caesium-137 in rats of various ages.
Health Phys., 18, 43-52.
Stradling, G.N., Pellow, P.G., Hodgson, A., Fell, T.P., Phipps, A., Pearce, M., Rance, E., Ellender,M., Taskaeva, M., Penev, I., Guentchev, T., 1996. Dose coefficient and assessment of intake
of a radionuclide bearing dust formed at the Kozloduy Nuclear Power Plant, NRPB-M679,
Chilton.
Stradling, G.N., Pellow, P.G., Hodgson, A., Fell, T.P., Phipps, A., Pearce, M., Taskaeva, M., Penev,
I., Guentchev, T., 1997. Assessment of intake of a complex radionuclide bearing dust formed
at a nuclear power plant. J. Radioanal. Nucl. Chem., 226(1-2), 7-14.
Stradling, G.N., Stather, J.W., Gray, S.A., Moody, J.C., Ellender M., Collier, C.G., 1989. Assessmentof intake of an actinide-bearing dust formed from the pond storage of spent magnox fuel.
Radiat. Prot. Dosim., 26, 201–206.
Talbot, R.J., Newton, D., Segal, M.G., 1993. Gastrointestinal absorption by rats of Cs-137 and Sr-90
from uranium octoxide fuel particles: implications for radiation doses to man after a nuclear
accident. Radiat. Prot. Dosim. 50: 39-43.
Thomas, R.G., Thomas, R.L., 1968. Long-term retention of Cs-137 in the rat. Health Phys., 15, 83-84.
Thomas, R.L., 1969, Deposition and initial translocation of inhaled particles in small laboratory
animals. Health Phys., 16, 417-428.
Thornberg, C., Mattsson, S., 2000. Increased 137Cs metabolism during pregnancy. Health Phys., 78,
502-506.
Wasserman, R.H., Wardock, A.R., Comar, C.L., 1959. Metabolic dissociation of short-lived barium137m from its caesium-137 parent. Science 129:568-569.
Williams, L.R., Leggett, R.W., 1987. The distribution of intracellular alkali metals in Reference Man.
Phys. Med. Biol. 32, 173-190.
Yamagata, N., 1962. Balance of potassium, rubidium, and caesium between Japanese people and dietand assessments of their biological half-times, Nature, 196, 83-84.
Yamagata, N., Iwashima, K., Nagai, T., Watari, K., Iinuma, T.A., 1966. In vivo experiment on themetabolism of caesium in human blood with reference to rubidium and potassium. J. Radiat.
Res., 7, 29-46.
Yano, Y., Van Dyke, D., Budinger, T.F., Anger, H.O., Chu, P., 1970. Myocardial uptake studies with
129
Cs and the scintillation camera. J. Nucl. Med., 11, 663-668.
Zundel, W.S., Tyler, F.H., Mays, C.W., Lloyd, R.D., Wagner, W.W., Pendleton, R.C., 1969. Shorthalf-times of caesium-137 in pregnant women. Nature, 221, 89-90.

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7. BARIUM (Z = 56)
7.1.

Chemical Forms in the Workplace(312) Barium is an alkaline earth element, which mainly occurs in oxidation states II. It is achemical analogue of calcium. Chemical forms encountered in industry include simple
inorganic salts such as chlorides, sulphates and carbonates. Barium sulphate is used as an Xray radiocontrast agent for imaging the human gastrointestinal tract. 133Ba is routinely used asa standard source in the calibration of gamma-ray detectors in nuclear physics studies.
Table 7-1. Isotopes of barium addressed in this report
IsotopeBa-124
Ba-126
Ba-127
Ba-128
Ba-129Ba-129m
Ba-131
Ba-131m
Ba-133aBa-133m
Ba-135m
Ba-139Ba-140aBa-141
Ba-142

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a

7.2.

Physical half-life
11.0 m100 m
12.7 m2.43 d2.23 h2.16 h
11.50 d14.6 m10.52 y38.9 h28.7 h83.06 m12.752 d
18.27 m10.6 mDecay mode
EC, B+
EC, B+
EC, B+EC
EC, B+
EC, B+EC
IT
EC
IT, ECITBBBB-Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

Routes of Intake

7.2.1. Inhalation
Absorption Types and parameter values(313) No direct information was found on the behaviour of inhaled barium in man.
Information is available from experimental studies of barium as chloride, sulphate or in fusedaluminosilicate particles (FAP).
(314) Absorption parameter values and Types, and associated fA values for particulate
forms of barium are given in Table 7-2.
Barium chloride(315) Cember et al. (1961) reported that more than 99% of barium administered to rats byintratracheal injection of 133BaCl2 had cleared from the lungs within 3 hours. Cuddihy and
Griffith (1972) observed very rapid, and almost complete, absorption of 140BaCl2 following
inhalation of 140Ba–140La by dogs, consistent with assignment to Type F. They developed abiokinetic model to represent the results, and with it estimated a rate of transfer of Ba from110

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the respiratory tract to blood of 25 d–1 (t½ ~ 40 minutes). In the model, a small fraction(0.3%) of the deposit in the pulmonary region was retained indefinitely. This was notdiscussed: it could represent a small “bound” component, or systemic barium in lung tissues
and blood. In a complementary experiment, alimentary tract absorption of 140Ba following
administration of 140BaCl2 to dogs by gavage was 7%. However, Cuddihy and Griffith notedthat reported values of alimentary tract absorption reported in the literature for BaCl2 varied
greatly. In subsequent studies (Cuddihy et al., 1974) of dogs that inhaled 133BaCl2, essentiallyall of the existing body content was measured in the skeleton 16 d after the exposure. In vitro
dissolution of the same material showed >99.9% dissolved at a rate of 14 d–1 (t½ ~ 1 hour).
Cuddihy and Ozog (1973) deposited 140BaCl2 directly onto the nasal membranes of Syrian
hamsters: the results give an absorption rate of about 7 d–1 (t½ ~ 2 hours). This is somewhat
slower than in other studies, possibly because of the experimental techniques used, including
the anaesthetic or slower clearance from the nasal passage than from the lungs. Similar
observations were made for strontium and caesium chlorides which were also administered by
Cuddihy and Ozog (see Strontium and Caesium Sections).
(316) Based on the results of the experiments outlined above, specific absorption
parameter values for barium chloride were estimated by the Task group to be: fr = 1 andsr = 20 d-1 (consistent with assignment to default Type F). However, although specificparameter values for barium chloride based on in vivo data are available, they are not adopted
here, because inhalation exposure to it is so unlikely. Instead, barium chloride is assigned toType F. However, the data are used as the basis for the default rapid dissolution rate forbarium. Hence specific parameter values for barium chloride would be the same as default
Type F barium parameter values.
Barium carbonate(317) For details see the section on carbon. Measurements of lung retention of 14C
following pulmonary intubation of barium 14C-labelled carbonate into rats, and accidental
inhalation by man, indicate assignment to Type F.
Barium sulphate.
(318) Morrow et al. (1964) observed a biological half time in the lungs of 8 d following
inhalation of 131BaSO4 by a dog, corresponding to a rate of absorption of about 0.1 d–1, andassignment to Type F. Cuddihy et al. (1974) followed the behaviour of 133Ba for 16 d after
inhalation of 133BaSO4 by dogs. In vitro dissolution tests of the same material gave fr = 0.9, sr= 0.4 d–1 (t½ ~ 2 d) and ss = 0.0017 d–1 (t½ ~ 400 d), consistent with absorption Type F. These
values were incorporated in a biokinetic model, which gave predictions in good agreementwith the observed in vivo behaviour. In similar experiments with heat-treated (900˚C)
133
BaSO4 (Cuddihy et al., 1974), in vitro dissolution tests gave fr = 0.2, sr = 0.07 d–1 (t½ ~ 10d) and ss = 0.038 d–1 (t½ ~ 18 d), consistent with absorption Type M. Again, biokinetic model
predictions using these values were in reasonable agreement with the observed behaviour.
(319) 133BaSO4 has also been used as an effectively insoluble test material to study theretention and clearance of particles deposited in the trachea in several species (Patrick andStirling, 1977; Takahashi and Patrick, 1987; Takahashi et al., 1993; Patrick and Stirling,1997). Most of these studies were of short duration (typically a week), and absorption was
not considered to be a significant clearance pathway. In one, however, measurements weremade for 6 months, and included tissue distribution data, which indicate Type M behaviour(Takahashi and Patrick, 1987). In rats, about 1% of the material deposited on the distal

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trachea was retained with a half-time of 88 days, and the main clearance route identified wasto lymph nodes, suggesting an absorption rate of less than 0.01 d–1.
(320) Overall, a wide range of absorption rates has been observed, possibly due todifferences in the method of preparation of the BaSO4. Specific parameter values are
therefore not proposed and BaSO4 is assigned to Type M.
Fused aluminosilicate particles (FAP)(321) FAP or “fused clay” particles have been extensively used as relatively insoluble
particles in inhalation studies, both of biokinetics and of radiation effects. A natural clay
mineral is labelled by ion exchange, and the labelled clay particles heated to about 1100˚C, toform aluminosilicate glass microspheres in which the label is incorporated. Cuddihy et al.
(1974) followed the behaviour of 133Ba for 512 d after inhalation of 133Ba-FAP by dogs. In
vitro dissolution tests (duration 120 d) of the same material gave fr = 0.12, sr = 0.13 d–1 (t½ ~ 5d) and ss = 0.0016 d–1 (t½ ~ 430 d), consistent with absorption Type M. These wereincorporated in a biokinetic model, which gave predictions in good agreement with theobserved behaviour.
Rapid dissolution rate for barium(322) Studies with barium chloride outlined above give values of sr of about 20 d–1, which
is applied here to all Type F forms of barium.
Extent of binding of barium to the respiratory tract(323) Evidence from the barium chloride studies outlined above suggests that there is
probably little binding of barium. It is therefore assumed that for barium the bound state canbe neglected, i.e. fb = 0.0.

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Table 7-2. Absorption parameter values for inhaled and ingested barium
Inhaled particulate materials
Default parameter valuesb,cAbsorption Type Assigned forms
F
Barium chloride, carbonate
M
Barium sulphate; all unspecified
formsd
S
—

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Absorption
parameter
valuesafr
sr (d–1) ss (d–1)

Absorption fromthealimentarytract, fA

1
0.2

20
3

0.005

0.2
0.04

0.01

3

1x10-40.002

Ingested materials
Soluble forms
0.2
Insoluble form (sulphate, titanate)
1x10-4a
It is assumed that for barium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F formsof barium (20 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
bMaterials (e.g. barium chloride) are listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see text).
c
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type (or specific value where given) and the fA value for ingested soluble forms of barium (0.2).
dDefault Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

7.2.2. Ingestion(324) Barium absorption depends on its chemical form. Barium sulfate is poorly absorbed
from the gastrointestinal tract of adults (Figueroa et al., 1968; Boender and Verloop, 1969),
while acid-soluble barium salts (e.g. acetate, carbonate, chloride, nitrate, hydroxide…) arereadily dissolved in gastric acid and absorbed (Leggett, 1992a). Other factors are known toaffect absorption. In animals, fasting and low calcium concentration in the gut may increase
barium absorption by a factor 2 to 3 (Taylor et al., 1962, Della Rosa et al., 1967, Cuddihy and
Griffith, 1972).
(325) Figueroa et al. (1968) fed five patients with stable barium sulfate and recovered
97.7-103% of the barium given orally in the stools after 5 days. In another study using stablebarium sulfate and barium titanate, average urinary excretion by five to nine human subjects
during the 24h after oral intake varied from about 0.16 to 0.26 µg.g-1 ingested (Clavel et al.,1987) leading other authors to conclude that absorption of these forms should be in the orderof 10-4 (Leggett, 1992a).
(326) LeRoy et al. (1966) found the absorption of 133Ba from simulated fall-out to behighly variable. Absorption could only be detected by whole-body counting in 4 of the 8subjects and in these it varied between 0.01 and 0.15. The analysis of barium in humanexcreta (Harrison et al., 1956) suggested absorption of about 0.07 and the fraction of dietarybarium excreted in the urine of 2 subjects in a balance study was 0.02 and 0.06 (Tipton et al.,1969). In five female cancer patients with normal gut function, absorption of 140Ba added toorange juice as the chloride was about 0.08 with a range of 0.03 - 0.16. Studies in which theabsorption of Ba and Ra have been compared in rats, dogs, sheep, pigs and cows have shown
similar levels of absorption of the two elements (Garner, 1960; Taylor et al., 1962; Della
Rosa et al., 1967; Sansom and Garner, 1966).
(327) In Publication 30 (ICRP, 1979), absorption was taken to be 0.1 for all forms of Ba.

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However, as concluded by Leggett (1992a), absorption for soluble forms of barium may behigher. On the basis of chemical similarity with Ra, and similar absorption values reported forthe two elements, a value of 0.2 was adopted in Publication 67 (ICRP, 1993).
(328) An fA of 0.2 for adults is recommended here for direct ingestion of soluble forms ofbarium. For insoluble forms such as barium sulfate or titanate, an fA of 10-4 is recommended.
7.2.3. Systemic Distribution, Retention and Excretion
7.2.3.1. Summary of the database(329) The alkaline earth element barium is a physiological analogue of the alkaline earth
elements calcium, strontium, and radium but has different biokinetics from those elements
due to discrimination by biological membranes and hydroxyapatite crystals of bone. The
biokinetics of barium resembles that of radium much more closely than that of calcium orstrontium.
(330) Retention and distribution of barium have been determined in controlled studies
involving healthy human subjects (ICRP, 1973, 1993; Leggett, 1992a). There is also
information on the biokinetics of barium in other animal species (ICRP, 1993, Leggett,1992b). Data for human subjects or laboratory animals used in the development of the model
for systemic barium used in this report are summarized below in the discussion of the basis
for parameter values.
7.2.3.2. Biokinetic model for systemic barium(331) The generic model structure for bone-volume-seeking radionuclides was used in
ICRP Publication 67 (1993) to model the systemic biokinetics of barium. The same model
structure is applied in this report. The compartments and paths of movement as applied tobarium are summarized below.
(332) Blood plasma is treated as a uniformly mixed pool that contains all barium in bloodand exchanges activity with soft tissues and bone surfaces. Soft tissues are divided into threecompartments corresponding to fast, intermediate, and slow return of activity to plasma(compartments ST0, ST1, and ST2, respectively). The liver and kidneys are not addressed
separately in the model for barium but are included implicitly in the soft tissue compartments.
Bone is divided into cortical and trabecular bone, and each of these bone types is further
divided into bone surfaces and bone volume. Bone volume is viewed as consisting of two
pools, one that exchanges with activity in bone surface for a period of weeks or months and asecond, non-exchangeable pool from which activity can be removed only by bone
restructuring processes. Activity depositing in the skeleton is assigned to bone surface. Overa period of days a portion of the activity on bone surfaces moves to exchangeable bonevolume and the rest returns to plasma. Activity leaves exchangeable bone volume over a
period of months, with part of the activity moving to bone surfaces and the rest to nonexchangeable bone volume. The rate of removal from non-exchangeable bone volume isassumed to be the rate of bone turnover, with different turnover rates applying to cortical andtrabecular bone. Barium is assumed to be lost from the body only by urinary and fecal
excretion.
Parameter values(333) The parameter values for barium applied in ICRP Publication 67 (1993) to an adult
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member of the public are adopted in this document for application to workers. The basis forthe parameter values is summarized below.
(334) The biological behavior of injected or ingested barium has been investigated inseveral controlled studies involving human subjects (Bauer and Carlsson, 1957; Leroy et al.,
1966; Harrison et al., 1967; Harrison, 1981; Korsunskii et al., 1981; Newton et al., 1977,
1991, 2001) and several animal species (Richmond et al., 1960, 1962a, 1962b; Farnham andRowland, 1965; Ellsasser et al., 1969; Hardy et al., 1969; Wood et al., 1970; Cuddihy and
Griffith, 1972; Stather, 1974; Domanski et al., 1980). It has been shown that the biokinetics
of barium is similar but not identical to that of radium. For example, data for a healthy 60-yold male human injected with 223Ra and 133Ba indicate similar retention of these radionuclides
in blood and in the total body for several days after injection but a slightly more rapid declineof whole-body 223Ra after a few weeks (Harrison et al., 1967, Newton et al., 1977). In humanstudies, administered radium and barium isotopes have been excreted primarily in faeces(Schales, 1964; Harrison et al., 1967; Maletskos et al., 1969; Korsunskii et al., 1981) andhave shown fairly similar fecal excretion rates for at least a month after injection (Harrison etal., 1967). Barium appears to be eliminated in urine at a greater rate than radium (Harrison etal., 1967), but urinary excretion constitutes only a small fraction of total excretion of bothelements in humans (Harrison et al., 1967, Korsunskii et al., 1981, Newton et al., 1991). In a
study of the fate of 226Ra and 133Ba acutely ingested by eight beagles from 43 to 1500 days ofage, Della Rosa et al. (1967) found that these two radionuclides were absorbed and retainedwith nearly the same efficiency in each animal, with 30-d retention of barium being slightly
greater as an average than that of radium. In cows, radium and barium behaved similarly withregard to secretion into the gut, resorption from bone, and concentration in pigmented tissue
but differed in their rates of secretion into milk, loss in urine, and whole-body accretion(Sansom and Garner, 1966).
(335) Kinetic analysis of plasma disappearance curves for normal subjects intravenously
injected with radioisotopes of calcium, strontium, barium, or radium indicates that theseelements initially leave plasma at a rate of several hundred plasma volumes per day andequilibrate rapidly with an extravascular pool roughly three times the size of the plasma pool
(Heaney, 1964; Harrison et al., 1967; Hart and Spencer, 1976). Total transfer rates fromplasma of 70 d-1 yield reasonable fits to plasma disappearance curves for barium and radium
at times greater than 1-2 h after injection (Leggett, 1992a). The rapid early removal fromplasma is not addressed in this model.
(336) Fractional deposition of barium in the fast-turnover soft-tissue compartment ST0 is
determined as the balance after other deposition fractions have been assigned. As discussed
below, deposition fractions of 0.25 for bone, 0.1 for intermediate-term soft tissues (ST1),
0.002 for long-term soft tissues (ST2), and 0.32 for excretion pathways are assigned tobarium, leaving 0.328 for ST0. The derived transfer rate from plasma to ST0 is 0.328 x 70 d-1= 23 d-1. Based on the assumed relative amounts of barium in ST0 and plasma, the transfer
rate from ST0 to plasma is set at one-third the transfer rate from plasma to ST0, or 7.67 d-1.
(337) Data on intermediate-term retention of injected barium in human soft tissues arelargely qualitative but indicate that little barium remains in soft tissues by a few days after
injection (Korsunskii et al., 1981; Newton et al., 1991). This conclusion is consistent withdirect measurements of injected, ingested, or inhaled barium in tissues of laboratory animals(Garner, 1960; Loutit and Russell, 1961; Bligh and Taylor, 1963; Wood et al., 1970; Cuddihy
and Griffith, 1972). In vitro measurements indicate that barium competes with calcium fortransport across cell membranes and in some cases may be transported in preference overcalcium but may not be sequestered at intracellular sites that sequester calcium or strontium
115DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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4552
4553
4554
4555

(Mullins, 1959; Shine et al., 1978; Carafoli, 1987; Tsien et al., 1987). Comparative data on
the distributions of intravenously injected strontium and barium in rats (Bligh and Taylor
1963) indicate similar deposition of these elements in soft tissues but a much higher rate ofloss of barium than strontium from soft tissues. In this model it is assumed that barium isdeposited in the intermediate-term soft-tissue compartment ST1 to the same extent as calcium
or strontium (deposition fraction = 0.1) but returns to plasma at a much higher rate than thoseelements. A removal half-time of 1 d for barium is broadly consistent with soft-tissue data onlaboratory animals and qualitative information for human subjects. The derived transfer ratefrom plasma to ST1 is 0.1 x 70 d-1 = 7 d-1 and from ST1 to plasma is ln(2)/ 1 d = 0.693 d-1.
(338) Despite the low intermediate-term retention of injected barium in soft tissues, a nontrivial portion of total-body barium can be found in human soft tissues after chronic exposure(Schroeder et al., 1972; ICRP, 1973, 1975; Schlenker et al., 1982). Much of this may residein small, relatively insoluble deposits of barium sulphate (Garner, 1960; Schroeder et al.,
1972; Van Middlesworth and Robison, 1975; Doig, 1976). In this model, compartment ST2
is used to account for nearly all the barium in soft tissues during chronic intake. The
deposition fraction for compartment ST2 is set for consistency with the estimate that 4.7% of
total-body Ba resides in soft tissues of the average adult (Schlenker et al., 1982), taking
account of the projected contribution of ST1 and assuming that the removal half-time from
ST2 to plasma is the same as estimated for calcium (5 y). It is assumed that 0.2% of barium
leaving plasma enters ST2. The derived transfer rate from plasma to ST2 is 0.002 x 70 d-1 =0.14 d-1 and from ST2 to plasma is ln(2)/5 y = 0.00038 d-1.
(339) Data from human and animal studies indicate that the rate of loss of alkaline earth
elements from bone over the first few months after injection increases in the order calcium <strontium < barium < radium, and fractional long-term retention increases in the reverse
order. Some element-specific parameter values are required to account for these differences,
but most of the parameter values describing bone kinetics are generic, that is, the same foreach of these alkaline earth elements. The basis for applying generic values is discussed inearlier sections on calcium and strontium. Essentially, kinetic analysis of whole-bodyretention data for humans and more direct examination of alkaline earth kinetics in laboratory
animals do not reveal distinct differences between these elements with regard to thefollowing: early accumulation in bone as a fraction of activity reaching blood; initial division
between trabecular and cortical bone; early rate of loss from bone, interpreted for purposes ofthe present model as transfer from bone surfaces to plasma; the fraction subject tointermediate-term retention in bone, interpreted as transfer from bone surfaces toexchangeable bone volume; and the rate of removal from bone at times remote from uptake,interpreted as removal of non-exchangeable activity due to bone resorption. The following
generic parameter values are applied (see the earlier sections on calcium and strontium):
fractional deposition in bone = 0.25; fractional deposition in trabecular bone = 1.25 times thaton cortical bone; half-time on bone surface = 1 d, with 5/6 transferring to plasma and 1/6 toexchangeable bone volume; removal rate from non-exchangeable trabecular and cortical bonevolume = 18% and 3% y-1, respectively. The transfer rates for barium derived from thesegeneric parameter values are as follows: plasma to trabecular bone surface = (1.25/2.25) x
0.25 x 70 d-1 = 9.72 d-1; plasma to cortical bone surface = (1/2.25) x 0.25 x 70 d-1 = 7.78 d-1;
trabecular or cortical bone surface to the corresponding exchangeable bone volume
compartment = (1/6) × ln(2)/1 d = 0.116 d-1, trabecular or cortical bone surface to plasma is(5/6) × ln(2)/1 d = 0.578 d-1; trabecular bone volume to plasma, 0.000493 d-1; and nonexchangeable cortical bone volume to plasma, 0.0000821 d-1.

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4584
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4591
4592
4593

(340) Observed differences in the behavior of alkaline earth elements in bone are accounted
for by differences in the rate of removal from the exchangeable bone volume compartments andthe fraction transferred from exchangeable to non-exchangeable bone volume. It is assumed, in
effect, that calcium, strontium, barium, and radium are all equally likely to become temporarily
incorporated in bone mineral after injection into blood but that the likelihood of reaching a nonexchangeable site in bone crystal decreases in the order calcium > strontium > barium > radium.
Fractional transfers of calcium, strontium, barium, and radium from exchangeable to nonexchangeable bone volume are set at 0.6, 0.5, 0.3, and 0.2, respectively, and the balance isassumed to return to bone surfaces. The removal half-times from exchangeable bone volume
are set at 100 d, 80 d, 50 d, and 30 d, respectively. These values are set to achieve reasonableconsistency with whole-body retention curves for humans injected with radioisotopes of thealkaline earth elements (e.g. Harrison et al., 1967; Newton et al., 1991). The assumed
fractional transfers to non-exchangeable bone volume are also reasonably consistent withresults of in vitro measurements. For example, under conditions approximating physiological,
Neuman (1964) found that calcium incorporated into forming hydroxyapatite crystals is 65%
non-exchangeable, and Stark (1968) determined discrimination factors relative to calcium of
0.93 for strontium, 0.56 for barium, and 0.32 for radium in forming crystals. Such in vitro
results have varied to some extent with experimental conditions, length of aging of the crystals,
and the definition of discrimination (Neuman, 1964; Stark, 1968).
(341) For barium, the above estimates of the removal half-time from exchangeable bonevolume and the fractional transfers to non-exchangeable bone volume and bone surface yield
the following transfer rates: exchangeable to non-exchangeable bone volume (cortical ortrabecular), 0.3 x ln(2)/50 d = 0.0042 d-1; exchangeable bone volume to bone surface, 0.7 x
ln(2)/50 d = 0.0097 d-1.
(342) Based on estimates from human studies (Harrison et al., 1967; Newton et al., 1991),
it is estimated that about 32% of barium leaving plasma is deposited in excretion pathways
and that the ratio of urinary to faecal excretion is about 1:9. The derived transfer rate fromplasma to the urinary bladder contents is 0.1 × 0.32 × 70 d-1 = 2.24 d-1 and from plasma to thecontents of the right colon is 0.9 × 0.32 × 70 d-1 = 20.16 d-1.
(343) Newton et al. (1991, 2001) conducted a long-term study of the biokinetics of 133Ba insix healthy adult male subjects. Data for the first ~3 y of that study were considered in thedevelopment of the systemic model (Leggett, 1992b) adopted in ICRP Publication 67 (1993)
and used in the present document. External measurements of whole-body retention of 133Ba
in each subject were continued until recently (Newton et al., 2001), providing a check onmodel predictions through ~13 y post injection. Model predictions are compared in Figure
6-1 with the reported data.

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4594
4595
4596
4597
4598
4599
4600
4601

Figure 7-1. Comparisons of measured whole-body retention of 133Ba intravenously
injected into six healthy men (Newton et al., 1991, 2001) with predictions of the systemic
biokinetic model adopted in ICRP Publication 67 (1993) and used in this report. Datafor the first ~3 y post injection were used in the construction of the model.
Table 7-3. Transfer rates (d-1) for barium.
Pathway
Plasma to urinary bladder contents
Plasma to right colon
Plasma to trabecular bone surface
Plasma to cortical bone surface
Plasma to ST0
Plasma to ST1
Plasma to ST2
Trabecular bone surface to plasma
Trabecular bone surface to exch volume
Cortical bone surface to plasma
Cortical bone surface to exchangeable volume
ST0 to Plasma
ST1 to Plasma
ST2 to Plasma
Exchangeable trabecular bone volume to surface
Exchangeable to nonexchangeable trabecular bone volume
Exchangeable cortical bone volume to surface
Exchangeable to nonexchangeable cortical bone volume
Nonexchangeable cortical bone volume to plasma
Nonexchangeable trabecular bone volume to plasma

4602

118

Transfer rate(d-1)
2.2400E+00
2.0160E+01
9.7200E+00
7.7800E+00
2.3000E+01
7.0000E+00
1.4000E-01
5.7800E-01
1.1600E-01
5.7800E-01
1.1600E-01
7.6700E+00
6.9300E-01
3.8000E-04
9.7000E-03
4.2000E-03
9.7000E-03
4.2000E-03
8.2100E-05
4.9300E-04

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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7.2.3.3. Treatment of radioactive progeny(344) Several of the barium isotopes addressed in this report have radioactive progeny that
may contribute significantly to dose coefficients for the internally deposited barium parent.
These progeny are isotopes of barium, caesium, lanthanum, or cerium.
(345) Barium, caesium, lanthanum, and cerium atoms produced in systemic compartments
by radioactive decay are assumed to follow the characteristic models for these elements (i.e.
the models applied in this report to these elements as parent radionuclides) from their time of
production, insofar as application of this assumption is straightforward. This assumption issometimes ambiguous due to differences in model structures for the different elements. Thatis, the site of production of a radionuclide may not be clearly identifiable with a specificcompartment in its characteristic model. In such cases a transfer rate from the site ofproduction of the radionuclide to the central blood compartment in the radionuclide’scharacteristic model has been assigned as described below. After reaching its central bloodcompartment, the radionuclide is assumed to behave as described by its characteristic model.
(346) A caesium atom produced in a soft tissue compartment of the barium model isassumed to transfer to the central blood compartment of the characteristic model for cesium at
the rate 1000 d-1, a default value used in this report to describe rapid biological transfer.
Caesium produced in a non-exchangeable bone compartment of the barium model transfers to
the central blood compartment at the rate of bone turnover. Caesium produced in bone surface
or exchangeable bone volume transfers to the central blood compartment at the rate ofremoval from bone surface compartments given in the characteristic model for caesium(0.212 d-1). A caesium atom produced in the blood compartment of the barium model isassumed to be produced in the central blood compartment of the characteristic model for
caesium.
(347) The characteristic model for lanthanum and cerium (the same model is applied toboth elements) will appear in a later part of this series. The reader is referred to a paper by
Taylor and Leggett (2003) for a description of the model. In this report, a lanthanum or
cerium atom produced in a soft-tissue compartment of the barium model is assumed totransfer to the blood compartment of the lanthanum/cerium model with a half-time of 0.5 d.
This is the shortest biological half-time for any soft tissue compartment in that model. A
lanthanum or cerium atom produced in a bone compartment of the barium model is assumed
to behave as if deposited in that compartment as a parent radionuclide. With regard to the
biokinetics of lanthanum or cerium, no distinction is made between production in an
exchangeable or a non-exchangeable bone volume compartment of the barium model. In
either case the assigned removal rate to the corresponding marrow compartment is the rate ofbone turnover.
7.3. Individual monitoring
133

Ba(348) Monitoring of 133Ba is usually accomplished through urine bioassay.

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4645

Isotope
133
133

4646
4647
4648
4649
4650

Ba
Ba

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
0.6 Bq/L
γ-ray spectrometry
Whole
Body γ-ray spectrometry 100 Bq
Counting

Achievabledetection limit
0.06 Bq/L
32 Bq

140

Ba
(349) Monitoring of 140Ba is usually accomplished through urine bioassay. Whole Body
Counting may also be used.
Isotope
140

Ba
Ba

140

4651
4652
4653
4654
4655
4656
4657
4658
4659
4660
4661
4662
4663
4664
4665
4666
4667
4668
4669
4670
4671
4672
4673
4674
4675
4676
4677
4678
4679
4680
4681

Monitoring
TechniqueMonitoring
Technique

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
1 Bq/L
γ-ray spectrometry
Whole
Body γ-ray spectrometry 80 Bq
Counting

Achievabledetection limit
0.1 Bq/L
51 Bq

References
Bauer, G.C.H., Carlsson, A., 1957. Lindquist, B. Metabolism of Ba-140 in man. Acta Orth. Scand.
26, 241-257.
Bligh, P.H., Taylor, D.M., 1963. Comparative studies of the metabolism of strontium and barium inthe rat. Biochem. J. 87, 612-618.
Boender, C.A., Verloop, M.C., 1969. Iron absorption, iron loss and iron retention in man: studies
after oral administration of a tracer dose of 59FeSO4 and 131-BaSO4. Br. J. Haematol., 17,45-58.
Carafoli, E., 1987. Intracellular calcium homeostasis Ann. Rev. Biochem. 56, 395-433.
Cember, Watson, J.A., Novak, M.E., 1961. The influence of radioactivity and lung burden on thepulmonary clearance rate of barium sulphate. Am. Ind. Hyg. Assoc. J., 22, 27–32.
Clavel, J.P., Lorillot, M.L., Buthiau, D., Gerbet, D., Heitz, F., Galli, A., 1987. Intestinal absorption of
barium during radiological studies. Therapie 42, 239-43.
Cuddihy, R.G., Ozog, J.A., 1973. Nasal absorption of CsCl, SrCl2, BaCl2 and CeCl3 in Syrian
hamsters. Health Phys., 25, 219–224.
Cuddihy, R.G., Griffith, W.C., 1972. A biological model describing tissue distribution and wholebody retention of barium and lanthanum in beagle dogs after inhalation and gavage. HealthPhys., 23, 621-633.
Cuddihy, R.G., Hall, R.P., Griffith, W.C., 1974. Inhalation exposure to barium aerosols: physical,
chemical and mathematical analysis. Health Phys., 26, 405–416.
Della Rosa, R.J., Goldman, M., Wolf, H.G., 1967. Uptake and retention of orally administered Ra226 and Ba-133: A preliminary report, University of California at Davis, Report 472-114,
pp. 40-41;
Doig, A.T., 1976. Baritosis: a benign pneumoconiosis. Thorax 31, 30-39.
Domanski, T., Witkowska, D., Garlicka, I., 1980. Influence of age on the discrimination of barium incomparison with strontium during their incorporation into compact bone. Acta Physiol. Pol.,31, 289-296.
Ellsasser, J.C., Farnham, J.E., Marshall, J.H., 1969. Comparative kinetics and autoradiography of Ca45 and Ba-133 in ten-year-old beagle dogs. J. Bone Jt. Surg. 51A, 1397-1412.

120

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
4682
4683
4684
4685
4686
4687
4688
4689
4690
4691
4692
4693
4694
4695
4696
4697
4698
4699
4700
4701
4702
4703
4704
4705
4706
4707
4708
4709
4710
4711
4712
4713
4714
4715
4716
4717
4718
4719
4720
4721
4722
4723
4724
4725
4726
4727
4728
4729
4730
4731
4732

Farnham, J.E., Rowland, R.E., 1965. The retention of Ba-133 in beagles. In: Radiological physics
division annual report, July 1964 through June 1965, Argonne National Laboratory; ANL7060; 70-73.
Figueroa, W.G., Jordan, T., Basset, S.H., 1968. Use of barium sulfate an an unabsorbable fecal
marker. Am. J. Cin. Nutr., 21, 1239-1245.
Garner, R.J., 1960. Distribution of radioactive barium in eye tissues. Nature 184, 733-734.
Hardy, E., Rivera, J., Fisenne, I., Pond, W., Hogue, D., 1969. Comparative utilization of dietaryradium-226 and other alkaline earths by pigs and sheep. In: Sikov, M.R., Mahlum, D.D.
(Eds.), Radiation biology of the fetal and juvenile mammal. Proc. 9th Annual Hanford
Biology Symposium at Richland, Washington, May 5-8, 1969. U.S. AEC, Division ofTechnical Information, 183-190.
Harrison, G.E., 1981. Whole body retention of the alkaline earths in adult man. Health Phys., 40, 9599.
Harrison, G.E., Carr, T.E.F., Sutton, A., 1967. Distribution of radioactive calcium, strontium, bariumand radium following intravenous injection into a healthy man. Int. J. Radiat. Biol., 13, 235247.
Harrison, G.E., Raymond, W.H.A., Tretheway, H.C., 1956. The estimation of barium and strontium
in biological materials by activation analysis with special reference to the turnover ofstrontium in man. In: Proc. International Conference on the Peaceful uses of Atomic
Energy. Vol. 11, Biological effects of radiation. New York, United Nations, 156-159.
Hart, H.E., Spencer, H., 1976. Vascular and extravascular calcium interchange in man determinedwith radioactive calcium. Radiat. Res., 67, 149-161.
Heaney, R.P., 1964. Evaluation and interpretation of calcium-kinetic data in man. Clin. Orthop. Rel.
Res., 31, 153-183.
ICRP, 1973. Alkaline Earth Metabolism in Adult Man. ICRP Publication 20, Pergamon Press,
Oxford.
ICRP, 1979. Limits on Intakes of Radionuclides for Workers. ICRP Publication 30, Pt.1. Ann. ICRP
2. (3/4).
ICRP, 1993. Age-dependent doses to members of the public from intake of radionuclides, Part 2.
Publication 67, Ann. ICRP 23(3/4).
Korsunskii, V.N., Tarasov, N.F., Naumenko, A.Z., 1981. Clinical evaluation of Ba-133m as an
osteotropic agent. ORNL/TR-86/30 (7 pgs); Translated from the Russian UDC 616.71-006073.916, Meditsinskaya Radiologiya No. 10, pp. 45-48.
Leggett, R.W., 1992a. Fractional absorption of ingested barium in adult humans. Health Phys., 62,
556-61.
Leggett, R.W., 1992b. A generic age-specific biokinetic model for calcium-like elements. Radiat.
Prot. Dosim., 41, 183-198.
LeRoy, G.V., Rust, J.H., Hasterlik, R.J., 1966. The consequences of ingestion by man of real andsimulated fallout. Health Phys., 12, 449-473.
Loutit, J.F., Russell, R.S., (Eds.), 1961. Progress in Nuclear Energy, Series VI, Biological Sciences.
Vol. 3, The entry of fission products into food chains. Pergamon Press, New York.
Maletskos, C.J., Keane, A.T., Telles, N.C., Evans, R.D., 1969. Retention and absorption of Ra-224
and Th-234 and some dosimetric considerations of Ra-224 in human beings. In: Mays,
C.W., Jee, W.S.S., Lloyd, R.D., Stover, B.J., Dougherty, J.H., Taylor, G.N. (Eds.), Delayed
effects of bone-seeking radionuclides, edSalt Lake City, UT. University of Utah Press, 2949.
Morrow, P.E., Gibb, F.R., Johnson, L., 1964. Clearance of insoluble dust from the lower respiratory
tract. Health Phys., 10, 443–555.
Mullins, L.J., 1959. The penetration of some cations into muscle. J. Gen. Physiol., 42, 817-829.
Neuman, W.F., 1964. Blood-bone exchange. In: Frost, H.M., (Ed.), Bone biodynamics, Boston, Little,
Brown, and Co, 393-408.

121

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
4733
4734
4735
4736
4737
4738
4739
4740
4741
4742
4743
4744
4745
4746
4747
4748
4749
4750
4751
4752
4753
4754
4755
4756
4757
4758
4759
4760
4761
4762
4763
4764
4765
4766
4767
4768
4769
4770
4771
4772
4773
4774
4775
4776
4777
4778
4779
4780
4781
4782
4783

Newton, D., Ancill, A.K., Naylor, K.E., Eastell, R., 2001. Long-term retention of injected barium-133
in man. Radiat. Prot. Dosim., 97, 231-240.
Newton, D., Harrison, G.E., Kang, C., Warner, A. J., 1991. Metabolism of injected barium in six
healthy men. Health Phys., 61, 191-201.
Newton, D., Rundo, J., Harrison, G.E., 1977. The retention of alkaline earth elements in man, withspecial reference to barium. Health Phys., 33, 45-53.
Patrick, G., Stirling, C., 1977. The retention of particles in large airways of the respiratory tract.
Proc. R. Soc. Lond. B., 198, 455–462.
Patrick, G., Stirling, C., 1997. Slow clearance of different-sized particles from rat trachea. J. Aero.
Med., 10, 55–65.
Richmond, C.R., Furchner, J.E., Trafton, G.H., 1962a. Retention and excretion of orally administered
Ba-133 by mice. Los Alamos Scientific Laboratory Report LAMS-2780, 17-25.
Richmond, C.R., Furchner, J.E., Trafton, G.H., 1962b. Retention and excretion of orally administered
Ba-133 by rats. Los Alamos Scientific Laboratory Report LAMS-2780, 26-34.
Richmond, C.R., Furchner, J.E., Trafton, G.H., 1960. Retention of Ba-133 in mice, rats, and dogs.
Los Alamos Scientific Laboratory Report LAMS-2455, 24-31.
Sansom, B.F., Garner, R.J., 1966. The metabolism of radium in dairy cows. Biochem. J. 99, 677-81.
Schales, F., 1964. The excretion of thorium X and its daughter products after intravenous injection inman. In: Assessment of radioactivity in man, Vol. II, Vienna, IAEA, 267-276.
Schlenker, R.A., Keane, A.T., Holtzman, R.B., 1982. The retention of Ra-226 in human soft tissue
and bone; implications for the ICRP 20 alkaline earth model. Health Phys., 42, 671-693.
Schroeder, H.A., Tipton, I.H., Nason, A.P., 1972. Trace metals in man: strontium and barium. J.
Chron. Dis., 25, 491-517.
Shine, K.I., Douglas, A.M., Ricchiuti, N.V., 1978. Calcium, strontium, and barium movements during
ischemia and reperfusion in rabbit ventricle. Circ. Res., 43, 712-720.
Stark, G., 1968. Studies on synthetic hydroxyapatite crystals with regard to metabolism of calcium,
strontium, barium and radium in bone. I. The discrimination against calcium. Biophysik., 5,42-54.
Stather, J.W., 1974. Distribution of P-32, Ca-45, Sr-85 and Ba-133 as a function of age in the mouseskeleton. Health Phys., 26, 71-79.
Takahashi, S., Patrick, G., 1987. Long term retention of 133Ba in the rat trachea following local
administration as barium sulfate particles. Radiat. Res., 110, 321–328.
Takahashi, S., Kubota, Y., Sato, H., Matsuoka, O., 1993. Retention of 133Ba in the trachea of rabbits,
dogs and monkeys following local administration of 133BaSO4 particles. Inhalation
Toxicology 5, 265–273.
Taylor, D.M., Bligh, P.H., Duggan, M.H., 1962. The absorption of calcium, strontium, barium, andradium from the gastrointestinal tract of the rat. Biochem. J., 83, 25-29.
Taylor, D.M., Leggett, R.W. 2003. A generic biokinetic model for predicting the behaviour of thelanthanide elements in the human body. Radiat. Prot. Dosimetry, 105, 193-198.
Tipton, I.H., Stewart, P.L., Dickson, J., 1969. Patterns of elemental excretion in long term balance
studies. Health Phys., 16, 455-462.
Tsien, R.W., Hess, P., McCleskey, E.W., Rosenberg, R.L., 1987. Calcium channels: Mechanisms of
selectivity, permeation, and block. Ann. Rev. Biophys. Biophys. Chem., 16, 265-290.
Van Middlesworth, L., Robison, W.L., 1975. Thyroid concentration of barium and radium. Int. J.
Nucl. Med. Biol., 2, 1-4.
Wood, S.K., Farnham, J. E., Marshall, J.H., 1970. Ca-45, Ba-133, and Ra-226 in 6-to 10-year-old
beagle dogs: A 100-day study. In: Radiological Physics Division annual report, Center for
Human Radiobiology, July 1969 through June 1970; Argonne, IL: Argonne National
Laboratory; ANL-7760, Part II, Biology and Medicine, 110-132.

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4796
4797

8. IRIDIUM (Z = 77)
8.1.

Chemical Forms in the Workplace(350) Iridium is a transition metal, which occurs mainly in oxidation states III and IV.
Iridium may be encountered in industry in a variety of chemical and physical forms, includingoxides (IrO2, Ir2O3), chlorides and fluorides. Iridium also forms a number of organometallic
compounds, such as iridium carbonyl.
(351) Iridium-192 is used as a gamma radiation brachytherapy source for the treatment ofcancer.
Table 8-1. Isotopes of iridium addressed in this report
Isotope
Ir-182
Ir-183
Ir-184
Ir-185
Ir-186
Ir-186m
Ir-187
Ir-188
Ir-189Ir-190Ir-190m
Ir-190n
Ir-192a
Ir-192n
Ir-193m
Ir-194Ir-194m
Ir-195
Ir-195m
Ir-196m

4798
4799
4800
4801
4802
4803
4804
4805
4806
4807
4808
4809
4810
4811
4812

a

8.2.

Physical half-life
15 m
58 m
3.09 h
14.4 h
16.64 h1.92 h10.5 h41.5 h13.2 d11.78 d1.12 h
3.087 h73.827 d
241 y10.53 d19.28 h
171 d
2.5 h
3.8 h
1.40 hDecay mode
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+, IT
EC, B+
EC, B+EC
EC
IT
EC, IT
B-, ECIT
IT
BBBB-, IT
B-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

Routes of Intake

8.2.1. Inhalation
Absorption Types and parameter values(352) Some information was found on the behaviour of inhaled iridium in man following
accidental intakes. Information is available from experimental studies of iridium chloride andelemental iridium.
(353) Absorption parameter values and Types, and associated fA values for particulate
forms of iridium are given in Table 8-2.
Iridium chloride
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4821
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4823
4824
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4826
4827
4828
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4831
4832
4833
4834
4835
4836
4837
4838
4839
4840
4841
4842
4843
4844
4845
4846
4847
4848
4849
4850
4851
4852
4853
4854
4855
4856
4857
4858
4859
4860

(354) Kreyling et al. (2002) followed the biokinetics of 192Ir for 7 days after intratracheal
instillation of 192IrCl3 into rats. By 7 days, about 8% of the initial lung deposit (ILD)
remained in the lungs, 10% ILD in soft tissues and bone, and smaller amounts in othertissues; 60% was excreted in urine and 10% in faeces (mostly in the first three days). Similar
results (unpublished) were obtained following inhalation (Kreyling, 2010). Analysis here
gave fr approximately 0.9. There is insufficient information to estimate other parameter values
precisely, but the low fecal excretion suggests that the rapid dissolution rate is high comparedto particle transport rates from the upper respiratory tract, 100 d–1, or more. The results thus
indicate assignment to Type F.
Elemental iridium (metal/oxide)(355) Casarett et al. (1960) followed the biokinetics of 192Ir for 28 days after inhalation by
rats of the aerosol formed by nebulising an aqueous suspension of 192Ir-labelled iridium. They
estimated that about 95% of the initial deposit (ID) deposited in the upper respiratory tract.
Only about 0.2% ID was retained in the lungs after 2 days, clearing with a half-time of about
23 days. Immediately after inhalation about 5% ID was found in the carcass, which reduced
to about 0.5% by 14 days, with a corresponding increase in urinary excretion. These results
suggest that the rapid dissolution rate is high compared to the particle transport rate from theupper respiratory tract, 100 d–1, or more. On that assumption, analysis by the task group gave
fr approximately 0.1, indicating assignment to Type M or S.
(356) Kreyling and co-workers have used 192Ir-labelled particles produced with a spark
generator (an intermittent arc between two electrodes in argon) as relatively inert particles tostudy the biokinetics of inhaled ultrafine particles, especially particle transport pathways. The
aerosol, produced by evaporation and condensation, consists of agglomerates of primaryparticles of about 2-5 nm diameter. Analysis showed the iridium nanoparticles to be oxidisedat the surface (Szymczak et al., 2006). The aerosol was administered (via an endotrachealtube) to rats which were intubated and ventilated, to avoid extrathoracic deposition and to
optimize deep lung deposition. In a complementary experiment in which a suspension of theparticles was administered via the oesophagus, no detectable 192Ir was observed in urine(Kreyling et al., 2002), which suggests that fractional absorption from the alimentary tract fA<0.0001.
(357) Kreyling et al. (2002) followed the biokinetics of 192Ir for 7 days after inhalation (viaan endotracheal tube) by rats of 15-nm and 80-nm count median diameter (CMD)
agglomerates of 192Ir-labelled particles, or intratracheal instillation of a particle suspension(15-nm CMD). By 7 days after inhalation 47% and 36% of the deposited 15- and 80-nm
particles had cleared, predominantly to faeces. Following inhalation of both aerosols urinary
excretion by 7 days was ~2% ILD, and following instillation ~0.1% ILD. For both aerosols, a
few percent of the ILD was found in tissues other than the lung, but most of this 192Ir was
attributed to particle translocation, rather than dissolution. Semmler et al. (2004) followed
the biokinetics of 192Ir for 180 days after inhalation (via an endotracheal tube) of 15-nm CMD
agglomerates of 192Ir-labelled particles. As in the study by Kreyling et al. (2002), only small
fractions of ILD were found in tissues other than the lung, and most was attributed to particle
translocation. Based on these results, those of Kreyling et al. (2002), and unpublishedexcretion data (Kreyling, 2010) parameter values assessed here were fr = 0.0 and ss = 0.01 d–1,
giving assignment to Type M.
(358) Cool et al. (1979) followed lung retention and excretion of 192Ir for two years after
accidental inhalation of iridium aerosol (produced by cutting into a source) by two workers.
Biological retention half times assessed from lung retention and fecal excretion were in the
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4862
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4864
4865
4866
4867
4868
4869
4870
4871
4872
4873
4874
4875
4876
4877
4878
4879
4880
4881
4882
4883
4884
4885
4886
4887
4888
4889
4890

range 700 – 3000 days, and it was reported that urine samples showed only “low activity”,
indicating assignment to Type S.
(359) Whole-body retention of 192Ir was followed for four months after accidental
inhalation by a worker of aerosol (considered to be metal or oxide) produced by grinding the
tip of an electrode, which had been used to seal 192Ir sources for industrial radiography byelectro-welding (IAEA, 1999). Partial-body monitoring showed the highest count rate above
the chest. There was little clearance after 13 days, indicating assignment to Type S.
192

Ir-labelled carbon(360) Kreyling et al. (2009) produced carbon chain aggregates (~25-nm CMD) containinga small fraction (< 1%) of 192Ir ultrafine (2-5 nm) particles by spark discharge between an
192
Ir-labelled iridium electrode and a graphite rod. At 24 hours after inhalation (via an
endotracheal tube) by rats, particle translocation to tissues (measured by 192Ir activity) was
less than for 20-nm pure iridium (see above).
Rapid dissolution rate for iridium(361) The experimental information for iridium chloride and elemental iridium suggeststhat the rate is high compared to particle transport rates from the upper respiratory tract, 100
d–1, or more, but is insufficient to provide an estimate. There is therefore no justification forchoosing a rate different from the general default value of 30 d–1, which is applied here to allType F forms of iridium.
Extent of binding of iridium to the respiratory tract(362) Information from the iridium chloride study outlined above suggests that about 10%of iridium deposited in the lungs in soluble form is retained. However there is no evidence
that it is retained in the bound state rather than in particulate form. It is therefore assumed thatfor iridium the bound state can be neglected, i.e. fb = 0.0.
Table 8-2. Absorption parameter values for inhaled and ingested iridium

Inhaled particulate materials
Default parameter valuesb,cAbsorption Assigned forms
TypeF
Iridium chlorideM
All unspecified formsd
S
Elemental iridium
Ingested materials
All unspecified forms

Absorption parameter valuesa
frsr (d–1)
ss (d–1)

Absorption from thealimentary tract, fA

1
0.2

30
3

–
0.005

0.01
0.002

0.01

3

1x10-4

1x10-40.01

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4894
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4897
4898
4899
4900
4901
4902
4903
4904
4905
4906
4907
4908
4909
4910
4911
4912
4913
4914
4915
4916
4917
4918
4919
4920
4921
4922
4923
4924
4925
4926
4927
4928
4929
4930
4931
4932
4933
4934
4935
4936
4937
4938
4939

a

b

c

d

It is assumed that for iridium the bound state can be neglected i.e. fb = 0. The values of sr for Type F,
M and S forms of iridium (30, 3 and 3 d–1, respectively) are the general default values.
Materials (e.g. iridium chloride) are listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see text).
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport tothe alimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr forthe absorption Type and the fA value for ingested soluble forms of iridium (0.01).
Default Type M is recommended for use in the absence of specific information, i.e. if the form is
unknown, or if the form is known but there is no information available on the absorption of that form
from the respiratory tract.

8.2.2. Ingestion(363) No human data are available on the absorption of iridium from the gastrointestinal
tract.
(364) The fractional absorption of iridium, administered as chloride (Na2192IrCl6), hasbeen measured in several mammalian species (mouse, rat, monkey and dog) and ranged from0.01 in mice to about 0.04 in monkeys (Furchner et al., 1971).
(365) In Publication 30 (ICRP, 1979), an absorption value of 0.01 was recommended.
Since no new data on the gastrointestinal absorption seem to be available, an fA value of 0.01
is adopted here for all chemical forms.
8.2.3. Systemic Distribution, Retention and Excretion
8.2.3.1. Summary of the database
Data for human subjects(366) Data on the biokinetics of iridium in human subjects are primarily from cases ofaccidental inhalation of 192Ir (Cool et al., 1979; Kelsey and Mettler, 2001; Brodsky and Wald,
2004). The case studies provide little information on the systemic behavior of iridium.
Data for laboratory animals(367) Casarett et al. (1960) studied the biokinetics of acutely inhaled metallic 192Ir in rats.
The count median diameter of the particles was 0.07 μm with a geometric standard deviationof about 1.5. Several rats were sacrificed immediately after exposure for determination ofdeposition in the respiratory tract, and pairs of rats were sacrificed at 3 h after exposure and at
1, 3, 6, 9, 13, and 14 d after exposure. Excretion was measured in some animals up to 28 d.
Mean deposition in the respiratory tract was ~58% of the inhaled activity. More than 95% of
the deposition was in the upper respiratory tract. The half-time of the initial phase ofclearance was 2-4 h, and the half-time of a second phase was ~24 h. Activity was found in theliver in two rats immediately after exposure and in one rat at 3 h after exposure, amounting toabout 0.2-0.6% of the deposited amount. In other rats, no significant activity was found in theliver or other tissues excluding skin except for spleen in two rats (0.14% at time zero and
0.02% at 3 d) and bone in two rats (0.55% at time zero and 0.14% at 3 h). Small but
measurable activities were found in skin throughout the 28-day study. Urinary and fecal
excretion accounted for <4% and >96% of the deposited amount, respectively, over 28 days.
The urinary excretion rate averaged over 48-hour periods was on the order of 1%/day for 0-2
d, 0.1%/day for 10-12 d, and 0.01%/day for 26-28 d.
(368) Durbin et al. (1957, 1960) described the results of tracer studies with 190Ir or 192Ir in

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4944
4945
4946
4947
4948
4949
4950
4951
4952
4953
4954
4955
4956
4957
4958
4959
4960
4961
4962
4963
4964
4965
4966
4967
4968
4969
4970
4971
4972
4973
4974
4975
4976
4977
4978
4979
4980
4981
4982
4983
4984
4985
4986

rats. Kidney, liver, and spleen were the main deposition sites. Excretion was mainly in urine.
After intravenous injection 36% was excreted in urine in the first 4 h. At 1 d the liver,kidneys, bone, blood, and muscle of rats contained 19.3%, 4%, 3.1%, 6.4%, and 5.6% andexcretion accounted for 43.5% of the administered amount. By 33 d, 45% was excreted inurine and 35% in faeces, and about 12% remained in liver, skin, and muscle.
(369) Furchner et al. (1971) studied the systemic behavior of 192Ir in mice, rats, monkeys,
and dogs after oral administration, intravenous injection, or intraperitoneal injection of
Na2192IrCl6. Cumulative urinary excretion during the first two days after oral intake averaged
0.86% of the administered amount in mice, 2.02% in Mystromys rats, 0.96% in SpragueDawley rats, 1.34% in monkeys, and 3.54% in dogs. These results indicate that averagefractional uptake by the gastrointestinal tract was higher than the value 0.01 applied toiridium in ICRP Publication 68 (1994). Whole-body retention over several months following
intravenous or intraperitoneal injection was similar in dogs, mice, Mystromys rats, andSprague-Dawley rats (Figure 8-1). Monkeys showed lower excretion rates initially than dogs,
mice, or rats but a faster drop in the body burden than the other species at times remote frominjection (Figure 8-1). Whole-body retention in all species could be described in terms of
three components with average biological half-times on the order of a few hours, a week, andseveral months (120-375 d). On average the rapid phase of loss represented about 20% (927%) of the administered amount, compared with mean excretion of 43.5% in rats receiving
190
Ir or 192Ir chloride by intravenous injection as reported by Durbin (1960). The long-term
component represented at least 46% of the administered amount in all species. As illustrated
in Table 8-3, whole-body retention curves based on the different animal species and different
modes of injection give fairly similar cumulative activities in the body for iridium isotopes
with a range of half-lives. The distribution of activity was determined in rats over the first 120
d after intraperitoneal injection. The retention times in individual organs roughly paralleledthat in the whole body. Highest concentrations were found in spleen, kidneys, and liver, inthat order. The concentration in bone was a factor of 2-3 lower than that of liver but higher
than the average concentration in the body. The liver, kidneys, and bone contained roughly
15%, 5%, 1-2%, and 10% of total-body content, respectively, during the observation period.
The authors concluded from comparison with injection data of Durbin et al. (1957) for ratsthat the rate of loss of iridium from the body depends on the chemical form reaching blood.
(370) Ando et al. (1989) determined the distribution of 192Ir in rats at 3, 24, and 48 h after
intravenous injection of H2192IrCl6. Cumulative urinary excretion at 3 h represented 79.8% of
injected 192Ir. At all three observation times the highest concentration was found in thekidneys, followed by liver. In contrast to findings of Durbin et al. (1957) and Furchner et al.
(1971), the concentration of iridium in the spleen was an order of magnitude lower than thatof kidney and a factor of 3-4 lower than that of liver.
(371) Hirunuma et al. (1997) studied uptake, retention, and excretion of 17 trace elements
including iridium in Wistar rats over the first 6 d after oral intake of radioisotopes of theseelements in a hydrochloric acid solution. Iridium was found in liver, kidney, and intestinal
tissue, with the kidneys generally showing the highest concentration. Iridium was notdetectable by the multi-tracer technique in brain, skeletal muscle, bone, spleen, testes, or
blood. On Day 3 the liver, kidneys, and intestines contained about 0.35%, 0.26%, and 0.13%,
respectively, of the administered iridium. On Day 6 these three organs contained about
0.11%, 0.13%, and 0.04%, respectively, of the administered iridium. Over the 6-day study
about 90% of the administered iridium was excreted in faeces and 7.7% was excreted inurine, indicating that most of the absorbed iridium was excreted during the short study period.

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE

4987
4988
4989
4990
4991
4992

Figure 8-1. Whole-body retention of 192Ir in laboratory animals following intravenous (iv) or
intraperitoneal (ip) injection of Na2192IrCl6 (curve fits reported by Furchner et al., 1971). Curve 1 =dogs, iv injection, observation period 304 d; 2 = monkeys, iv, 227 d; 3 = mice, iv, 352 d; 4 = rats, iv,
280 d; 5 = mice, ip, 364 d; 6 = rats, ip, 371 d.
Table 8-3. Cumulative activities of iridium isotopes in the whole body based on retention
curves derived by Furchner et al. (1971). Values for a given isotope are normalized to
the value for that isotope in dogs.
Isotope
Ir-190Ir-192
Ir-192n
Ir-194
Ir194m
a

b

4993
4994
4995
4996
4997
4998
4999
5000
5001
5002
5003
5004
5005
5006
5007
5008

Half-life
11.78 d73.827 d241 y19.28 h
171 d

Dogsa
1.0
1.0
1.0
1.0
1.0

Monkeysa
1.3
1.2
0.8
1.1
1.1

Micea
1.0
1.1
1.7
1.0
1.2

Ratsa
1.1
1.0
0.8
1.0
1.0

Miceb
0.8
0.7
0.6
1.0
0.7

Ratsb
1.0
1.0
1.2
1.1
1.1

intravenous injection
intraperitoneal injection

8.2.3.2. Biokinetic model for systemic iridium(372) Biokinetic data for iridium summarized above indicate that whole-body retention is
not predictable on the basis of body size and does not vary greatly from one species toanother. Three phases of excretion of absorbed or intravenously injected iridium areindicated: a rapid phase of loss, primarily in urine, with a half-time of a few hours; anintermediate phase of loss with a half-time on the order of 1-2 wk; and a slow phase of loss
with a half-time of several months. The fraction of uptake associate with each of these phases
is variable and depends on the form of iridium reaching blood. For example, the fraction
associated with the rapid phase of loss in urine has varied from <0.1 to 0.8 or more. The rateof loss from individual tissues roughly parallels that in the whole body. Concentrations of
iridium in the kidneys and liver are much higher than those in most other tissues. Elevateduptake of iridium by the spleen is indicated by some data, but findings are inconsistent. Dataon rats indicate that the liver contains roughly 15-20% of the systemic content during the firstfew months after input to blood. Most studies indicate that kidneys and bone accumulate less

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5009
5010
5011
5012
5013
5014

5015
5016
5017

iridium than does the liver.
(373) The structure of the biokinetic model for systemic iridium is shown in Figure 8-2.
Transfer coefficients are listed in Table 8-4. Whole-body retention data of Furchner et al.
(1971) for dogs were used as a guide for model parameters. The retention data for dogs are
typical of the studied species.

Figure 8-2. Structure of the biokinetic model for systemic iridium.

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5018

Table 8-4. Transfer coefficients for systemic iridium

5019
5020
5021
5022
5023
5024
5025
5026
5027
5028
5029
5030
5031
5032
5033
5034
5035
5036

From

To

Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 2
Liver 1
Liver 1
Liver 1
Liver 2Urinary path
Other kidney tissue
ST0
ST1
ST2
Cortical bone surface
Trabecular bone surface
Cortical bone surface
Trabecular bone surface
Cortical bone volume
Trabecular bone volume

Small intestine contents
Urinary bladder contents
Liver 1
Urinary path
Other kidney tissue
Blood 2
ST0
ST1
ST2
Cortical bone surface
Trabecular bone surface
Blood 1
Blood 1
Small intestine contents
Liver 2
Blood 1
Urinary bladder contents
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Blood 1
Cortical bone volume
Trabecular bone volume
Blood 1
Blood 1

Transfercoefficient (d-1)
4.0
12
12
4.0
2.0
27
15
15
1.0
4.0
4.0
0.693
0.0231
0.04620.06930.00693
0.139
0.006930.06930.006930.00095
0.01850.01850.004620.004620.0000821
0.000493(374) In the model for iridium, urinary excretion is assumed to arise from transfer ofactivity from blood into the urinary bladder contents and transfer from blood to the kidneys(Urinary path) and subsequent release to the urinary bladder contents over a period of days.
Fecal excretion is assumed to arise in part from biliary secretion into Small intestine contentsfrom a liver compartment (Liver 1) and in part from secretion from Blood 1 into Small
intestine contents. The parameter values are set so that the two sources of faecal excretion
contribute equally to endogenous faecal excretion of iridium, in the absence of specific dataon relative contributions of these sources. Deposition fractions and removal half-times forcompartments are set to reproduce different phases of loss of iridium from the total bodyobserved in laboratory animals.
(375) Clearance of iridium from blood is modeled on the basis of human data for thechemically related element ruthenium (Veronese et al., 2003, 2004). Blood is divided into two
compartments called Blood 1 and Blood 2. Iridium entering blood is assigned to Blood 1,
which is a rapid-turnover pool. Blood 2 is a more slowly exchanging pool that contains the
preponderance of activity in blood except for a short period soon after acute uptake of
iridium. Activity leaves Blood 1 at the rate 100 d-1, corresponding to a half-time of ~10 min,with 27% of outflow going to Blood 2 and the remaining 73% divided among tissue130

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5038
5039
5040
5041
5042
5043
5044
5045
5046
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5048
5049
5050
5051
5052
5053
5054
5055
5056
5057
5058
5059
5060

5061
5062
5063
5064
5065
5066
5067

compartments, urinary bladder contents, and gastrointestinal contents. Activity moves from
Blood 2 back to Blood 1 with a half-time of 1 d.
(376) In addition to the 27% of outflow from Blood 1 assigned to Blood 2, outflow from
Blood 1 is assumed to be distributed as follows: 12% to Liver, 6% to Kidneys, 8% to Bone,
12% to the Urinary bladder contents, 4% to Small intestine contents, and the remainder (31%)
to Other. Activity entering Liver is assigned to a compartment called Liver 1 that has
relatively fast turnover. Two-thirds of the activity entering Kidneys (4% of outflow from
Blood 1) is assigned to Urinary path and one-third (2%) to Other kidney tissue; thus, a total of
12% + 4% = 16% of activity leaving Blood 1 enters the urinary excretion pathways. Activity
depositing in bone is divided equally between Cortical bone surface and Trabecular bone
surface. Activity entering Other is divided as follows: fast-turnover compartment ST0, 15%;
intermediate turnover compartment ST1, 15%; and slow-turnover compartment ST2, 1%.
(377) Activity transfers from Liver 1 with a half-time of 5 d, with one-third going to the
Small intestine contents (biliary secretion), one-half to Liver 2, and one-sixth to Blood 1.
Activity transfers from Liver 2 to Blood 1 with a half-time of 100 d. Activity transfers from
Urinary path to Urinary bladder contents with a half-time of 5 d and from Other kidney
tissues to Blood 1 with a half-time of 100 d. Activity in soft-tissue compartments ST0, ST1,and ST2 returns to Blood 1 with half-times of 10 d, 100 d, and 2 y, respectively. Activity
leaves Cortical and Trabecular bone surface with a half-time of 30 d, with 80% returning to
Blood 1 and 20% entering the corresponding bone volume compartment. Activity istransferred from the bone volume compartments to Blood 1 at the rate of bone turnover.
(378) As illustrated in Figure 8-3, model predictions approximate whole-body retention of
iridium as determined in dogs after intravenous injection with 192Ir (Furchner et al., 1971).

Figure 8-3. Comparison of model predictions of whole-body retention of iridium withobservations for dogs. Data points derived from whole-body retention curve reported by Furchner etal. (1971) for dogs intravenously injected with Na2192IrCl6.

8.2.3.3. Treatment of radioactive progeny

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5069
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5072
5073
5074
5075
5076
5077
5078
5079
5080
5081
5082
5083
5084
5085
5086
5087
5088
5089
5090
5091
5092
5093
5094
5095
5096
5097
5098
5099
5100
5101
5102
5103
5104
5105
5106
5107
5108
5109
5110
5111
5112
5113
5114
5115

(379) Chain members addressed in the derivation of dose coefficients for isotopes of
iridium are isotopes of platinum, osmium, and rhenium. Independent kinetics of chain
members is assumed.
(380) Platinum and osmium are members of the platinum group, which also contains
iridium, ruthenium, rhodium, and palladium. These six metals are chemically similar andgenerally are found together in ores.
(381) The systemic biokinetics of ingested, inhaled, or injected platinum has been studied
in laboratory animals, mainly rats, and to some extent in human subjects (Durbin et al., 1957;
Durbin, 1960; Lange et al., 1973; Smith and Taylor, 1974; Litterst et al., 1976; Yoakum et al.,
1975; Moore et al., 1975a,b,c; Hirunuma et al., 1997). Platinum shows a high rate of urinary
excretion in the early days after administration. Some but not all studies also indicate a
relatively high rate of faecal excretion. Following intravenous administration of platinum
isotopes as the chloride to rats, highest concentrations generally were found in the kidneys,
followed by the liver (Durbin et al., 1957; Moore et al., 1975a,b,c). At 1 mo the rats
contained roughly 10-15% of the intravenously injected activity.
(382) Biokinetic studies of platinum in human subjects have focused on the behavior of theantitumor agent cis-diamminedichloroplatinum (II) (DDP) (Lange et al., 1973; Smith andTaylor, 1974). In these studies the biokinetics of the platinum label was similar to the
behavior of other forms of platinum following their administration to laboratory animals.
Following intravenous administration of 195mPt-labeled DDP to two cancer patients,
approximately 35% of the injected activity was excreted in urine during the first 3.5 d (Smith
and Taylor, 1974). At most a few percent of the activity was excreted in faeces during thattime. Based on external measurements, the liver accumulated an estimated 10% of theinjected activity during the first day. The biological removal half-times of activity from theliver and total body from days 1-7 were estimated as 8 d and 10 d, respectively. The study
period was too short to determine any longer-term components of retention.
(383) Biokinetic studies on rodents (Durbin et al., 1957; Durbin, 1960; Weininger et al.,
1990; Jamre et al., 2011) indicate that the systemic behavior of osmium is broadly similar tothat of platinum and the other members of the platinum group. The systemic distribution of
osmium at 1 d after intravenous injection closely resembled that of platinum (Durbin et al.,1957; Durbin, 1960). Highest concentrations of intravenously injected osmium and generally
occur in the kidneys and liver. Excretion of osmium is primarily in urine. Durbin andworkers (Durbin et al., 1957; Durbin, 1960) found that the rate of excretion of osmium wasinitially higher than that of other members of the platinum group. This may reflect
differences in the administered forms of these elements or experimental conditions; osmium
was administered as NaHOsO5 or OsO4, while the other elements were administered as
chloride compounds. Also, studies on mice indicate that the excretion rate of osmium
depends on the pH of the injected solution, with longest retention observed at relatively low
pH (Weininger et al., 1990). The total-body retention curves over the first four weeks
following intravenous administration of osmium to mice at relatively low pH (4.5-5.1) weresimilar to the retention pattern observed by Moore et al. (1975a,b,c) for systemic platinum inrats.
(384) In this report the same biokinetic model is applied to both osmium and platinum asprogeny of systemic iridium. The model is a modification of the characteristic biokinetic
model for ruthenium used in this report. The ruthenium model is modified by shifting a
portion of the deposition in bone and soft tissue compartments ST1 and ST2 to the urinary
bladder content and kidneys. Specifically, the ruthenium model is modified for application to
osmium and platinum as iridium progeny by the following changes in transfer coefficients:132

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5124
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5130
5131
5132
5133
5134
5135
5136
5137
5138
5139
5140
5141
5142
5143
5144

Blood 1 to Cortical bone surface, reduced from 6 d-1 to 3 d-1; Blood 1 to Trabecular bone
surface, reduced from 2 d-1 to 1 d-1; Blood 1 to ST1, reduced from 5 d-1 to 2.5 d-1; Blood 1 to
ST2, reduced from 5 d-1 to 2.5 d-1; Blood 1 to Urinary bladder content, increased from 17 d-1
to 23 d-1; Blood 1 to Kidneys 1 (urinary path), increased from 7.76 d-1 to 10.67 d-1; andBlood 1 to Kidneys 2 (other kidney tissue), increased from 0.24 d-1 to 0.33 d-1. These
modifications leave the total outflow rate from the central blood compartment, Blood 1,
unchanged at 100 d-1.
(385) An osmium or platinum atom produced by radioactive decay in a systemiccompartment is assigned the model for these elements described above from its time of
production. This is straightforward for osmium and platinum atoms because their preceding
chain members are also members of the platinum group, and all members of this group havethe same model structure. Each compartment in the model for osmium and platinum is
identified with the iridium compartment with the same name.
(386) Rhenium is a member of Group VIIA of the period table and exhibits chemical andbiokinetic properties remarkably close to those of the adjacent Group VIIA element
technetium (Durbin et al., 1957; Deutsch et al., 1986; Yanaga et al., 1996, Dadachova et al.,
2002; Zuckier et al., 2004). Rhenium and technetium presumably become covalently boundwith oxide ions to form the structurally similar anions perrhenate (ReO4-) and pertechnetate(TcO4-) in the body and in many environment settings. These two anions have important
medical applications as close physiological analogues of iodide, with the important exceptionthat there is little if any organic binding of perrhenate or pertechnetate in the thyroid. The
systemic biokinetic model applied in this report to technetium as a member of ruthenium
chains (see the section on ruthenium) is also applied to rhenium as a member of iridium
chains.
8.3. Individual monitoring(387) 192 Ir may be detected in urine or Whole Body counting.
Isotope
192

Ir
Ir

192

192

Ir

5145
5146
5147
5148
5149
5150
5151
5152
5153
5154
5155
5156
5157

Monitoring
Technique

MethodMeasurementof Typical
Detection
Limit
Urine Bioassay
γ-ray spectrometry
0.5Bq/L
Whole
Body γ-ray spectrometry
97Bq
Counting
Lung Monitoring
γ-ray spectrometry 6 Bq*

Achievabledetection limit∗ Lung monitoring of 192Ir is not generally used in routine monitoring of workers. Monte Carlo program
Visual Monte Carlo was used to simulate the photon emission, to calculate the calibration factor for thegeometry and radionuclide, and to calculate the minimum detectable activity (MDA) in the lung. (Hunt etal, 2012)

References
Ando, A., Ando, I., Hiraki, T., Hisada, K. 1989. Relation between the location of elements in the
periodic table and various organ-uptake rates. Nucl. Med. Biol. 16: 57-69.
Brodsky, A., Wald, N., 2004. Experiences with early emergency response and rules of thumb. In:
Brodsky, A.; Johnson, R.H., Jr., Goans, R.E., (Eds.), Public protection from nuclear,chemical, and biological terrorism. Health Physics Society 2004 Summer School. Madison,
Wisconsin: Medical Physics Publishing; 2004, Chapter 20, pp. 335-371.

133

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5159
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5161
5162
5163
5164
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5166
5167
5168
5169
5170
5171
5172
5173
5174
5175
5176
5177
5178
5179
5180
5181
5182
5183
5184
5185
5186
5187
5188
5189
5190
5191
5192
5193
5194
5195
5196
5197
5198
5199
5200
5201
5202
5203
5204
5205
5206
5207
5208
5209

Casarett, L.J., Bless, S., Katz, R., Scott, J.K., 1960. Retention and fate of iridium-192 in rats
following inhalation. J. Amer. Ind. Hyg. Assoc. 21, 414-418.
Cool, D.A., Cool, W.S., Brodsky, A., Eadie, G.G., 1979. Estimation of long-term biologicalelimination of insoluble iridium-192 from the human lung. Health Phys. 36, 629–632.
Dadachova, E.; Bouzahzah, B.; Zuckier, L. S.; Pestell, R. G. 2002. Rhenium-188 as an alternative toiodine-131 for treatment of breast tumors expressing the sodium/iodide symporter (NIS).
Nucl. Med. Biol. 29:13-18.
Deutsch, E.; Libson, K.; Vanderheyden, J. L.; Ketring, A. R.; Maxon, H. R. 1986. The chemistry ofrhenium and technetium as related to the use of isotopes of these elements in therapeuticand diagnostic nuclear medicine. Int. J. Rad. Appl. Instrum. B 13:465-477.
Durbin, P.W., 1960. Metabolic characteristics within a chemical family. Health Phys. 2, 225-238.
Durbin, P.W., Scott, K.G., Hamilton, J.G., 1957. Distribution of radioisotopes of some heavy metals
in the rat. University of California (Berkely) Publ. Pharmocol. 3, 1-34.
Furchner, J.E., Richmond, C.R., Drake, G.A., 1971. Comparative metabolism of radionuclides inmammals-V. Retention of 192Ir in the mouse, rat, monkey and dog. Health Phys. 20, 375382.
Hirunuma, R., Endo, K., Yanaga, M., Enomoto, S., Ambe, S., Tanaka, A., Tozawa, M., Ambe, F.,
1997) The use of a multitracer technique for the studies of the uptake and retention of traceelements in rats. Appl. Radiat. Isot. 48, 727-733.
IAEA, 1999. Intercomparison and biokinetic model validation of radionuclide intake assessment.
Case 6: Single intake of 192Ir. IAEA-TECDOC-1071 pp. 48-49.
ICRP, 1979. Limits on Intakes of Radionuclides for Workers. ICRP Publication 30, Part 2. Pergamon
Press, Oxford. Ann. ICRP 4 (3/4).
ICRP, 1994. Dose Coefficients for Intakes of Radionuclides by Workers. ICRP Publication 68. Ann.
ICRP 24(4).
Jamre, M.; Salek, N.; Jalilian, A. R.; Moghaddam, L.; Shamsaee, M.; Mazidi, M.; GhannadiMaragheh, M. 2011. Development of an in vivo radionuclide generator by labelingbleomycin with 191Os. J. Radioanal. Nucl. Chem. 290:543-549.
Kelsey, C.A., Mettler, Jr., F.A., 2001. Iridium-192 acid skin burn in Alburquerque, New Mexico,
U.S.A. Chapter 29. In: Gusev, I.A., Guskova, A.K., Mettler, Jr., F.A., (Eds.), Medical
management of radiation accidents, 2nd edition; New York: CRC Press, pp. 421-423.
Kreyling, W.G., 2010. Personal communication.
Kreyling, W.G., Semmler, M., Erbe, F., Mayer, P., Takanaka, S., Schulz, H., Oberdörster, G. andZiesenis, A., 2002. Translocation of ultrafine insoluble iridium particles from lungepithelium to extrapulmonary organs is size dependent but very low. Journal of Toxicology
and Environmental Health, Part A, 65 (20), 1513–1530.
Kreyling, W.G., Semmler-Behnke, M., Seitz, J., Scymczak, W., Wenk, A., Mayer, P., Takenaka, S.,
Oberdörster, G., 2009. Size dependence of the translocation of inhaled iridium and carbon
nanoparticles aggregates from the lungs of rats to the blood and secondary target organs.
Inhalation Toxicology, 21 (S1), 55–60.
Lange, R. C.; Spencer, R. P.; Harder, H. C. 1973. The anti-tumor agent cis-Pt(NH3)2Cl2: Distribution
studies and dose calculations for 193mPt and 195mPt. J. Nucl. Med. 14:191-195.
Litterst, C. L.; Gram, T. E.; Dedrick, R. L.; Leroy, A. F.; Guarino, A. M. 1976. Distribution anddispositionofplatinum
following
intravenous
administrationofcisdiamminedichloroplatinum (II) (NSC119875) to dogs. Cancer Res. 36:2340-2355.
Moore, W.; Hysell, D.; Crocker, W.; Stara, J. 1975a. Whole body retention in rats of different 191Pt
compounds following inhalation exposure. Environ. Health Persp. 12:35-39.
Moore, W.; Hysell, D.; Hall, L.; Campbell, K.; Stara, J. 1975b. Preliminary studies on the toxicity
and metabolism of palladium and platinum. Environ. Health Persp. 10:63-71.
Moore, W.; Malanchuk, M.; Crocker, W.; Hysell, D.; Cohen, A.; Stara, J. F. 1975c. Biological fate ofa single administration of 191Pt in rats following different routes of exposure. Environ Res.
9:152-158.

134

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5213
5214
5215
5216
5217
5218
5219
5220
5221
5222
5223
5224
5225
5226
5227
5228
5229
5230
5231
5232
5233
5234
5235
5236
5237
5238

Semmler, M., Seitz, J., Erbe, F., Mayer, P., Heyder, J., Oberdörster, G. and Kreyling, W.G., 2004.
Long-term clearance kinetics of inhaled ultrafine insoluble iridium particles from the rat
lung, including transient translocation into secondary organs. Inhal. Tox., 16, 453 – 459
Smith, P. H. S.; Taylor, D. M. 1974. Distribution and retention of the antitumor agent 195mPt-cisdichlorodiammine platinum (II) in man. J. Nucl. Med. 15:349-351.
Szymczak, W., Menzel, N., Kreyling, W.G., Wittmaack, K., 2006. TOF-SIMS characterisation of
spark-generated nanoparticles made from pairs of Ir–Ir and Ir–C electrodes. International
Journal of Mass Spectrometry 254, 70–84.
Veronese, I., Cantone, M.C., Giussani, A., Maggioni, T., Birattari, C., Bonardi, M., Groppi, F.,
Garlaschelli, L., Werner, E., Roth, P., Höllriegl, V., Louvat, P., Felgenhauer, N., Zilker, Th.,
2003. Stable tracer investigations in humans for assessing the biokinetics of ruthenium andzirconium radionuclides. Rad. Prot. Dosim. 105, 209–212.
Veronese, I., Giussani, A., Cantone, M.C., Birattari, C., Bonardi, M., Groppi, F., Höllriegl, V., Roth,P., Werner, E., 2004. Influence of the chemical form on the plasma clearance of ruthenium
in humans. Appl. Radiat. Isot. 60, 7-13.
Weininger, J.; Issachar, D.; Lubin, E.; Zabari, M.; Trumper, J. 1990. Influence of PH adjustment
agents on the biologic behavior of osmium-191 impurity in iridium-191m generator eluates.
J. Nucl. Med. 31:523-525.
Yanaga, M.; Enomoto, S.; Hirunuma, R.; Iuruta, R.; Endo, K.; Tanaka, A.; Ambe, S.; Tozawa, M.;
Ambe, F. (1996). Multitracer study on uptake and excretion of trace elements in rats. Appl.
Radiat. Isot. 47:235-246.
Yoakum, A. M.; Steward, P. L.; Sterrett, J. E. 1975. Method development and subsequent analysis of
biological tissues for platinum, lead and manganese content. Environ. Health Persp. 10:8593.
Zuckier, L. S.; Dohan, O.; Li, Y.; Chang, C. J.; Carrasco, N. ; Dadachova, E. 2004. Kinetics ofperrhenate uptake and comparative biodistribution of perrhenate, pertechnetate, and iodide
by NaI symporter-expressing tissues in vivo. J. Nucl. Med. 45:500-507.

135

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5241
5242
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5249
5250
5251
5252

9. Lead (Z = 82)
9.1.

Chemical Forms in the Workplace(388) Lead is a soft metal which mainly occurs in oxidation states II and IV. Lead may be
encountered in industry in a variety of chemical and physical forms, including oxides (PbO,
PbO2, Pb2O3, Pb3O4), chlorides, sulphides, fluorides, nitrates, and also as organic vapour
compounds (tetra-ethyl, tetra-methyl). Lead may also be present in uranium mines and mills.
Molten lead is used as a coolant in lead cooled fast reactors.
(389) 210Pb originates from the decay of 238U and 234Th, and 212Pb from the decay of 232Th.
Table 9-1. Isotopes of lead addressed in this report
IsotopePb-194
Pb-195m
Pb-196
Pb-197m
Pb-198
Pb-199
Pb-200Pb-201
Pb-202
Pb-202m
Pb-203
Pb-204m
Pb-205
Pb-209
Pb-210a
Pb-211
Pb-212aPb-214a

5253
5254
5255
5256
5257
5258
5259
5260
5261
5262
5263
5264
5265
5266
5267
5268

a

9.2.

Physical half-life
12 m
15 m
37 m
43 m
2.4 h
90 m
21.5 h
9.33 h
5.25E+4 y
3.53 h
51.873 h
67.2 m
1.53E+7 y3.253 h22.20 y36.1 m
10.64 h26.8 mDecay mode
EC, B+, A
EC, B+
EC,B+
EC, B+, IT
EC
EC, B+EC
EC, B+EC, A
IT, ECEC
IT
EC
BB-, ABBB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

Routes of Intake

9.2.1. Inhalation
Absorption Types and parameter values(390) Information is available from experimental studies of the behaviour of lead inhaledin a variety of forms by both animals and man. In particular, studies have been conducted to
improve assessment of risks from exposure to radioisotopes of lead inhaled as decay productsof radon, and from exposure to stable lead as an atmospheric pollutant, e.g. from petrolengine exhaust.
(391) Absorption parameter values and Types, and associated fA values for particulate
forms of lead are given in Table 9-2. Parameter values are not given for the gas and vapour
forms considered here because occupational exposure to radioisotopes in such forms is136

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5280
5281
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5283
5284
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5287
5288
5289
5290
5291
5292
5293
5294
5295
5296
5297
5298
5299
5300
5301
5302
5303
5304
5305
5306
5307
5308
5309
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5311
5312
5313
5314
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5316

unlikely. Exposures to gas and vapour forms of lead are relatively unusual compared to
exposures to particulate forms, and therefore it is proposed here that particulate form isassumed in the absence of information (ICRP, 2002b). However, for radiation protection
purposes, the most important exposures to radioisotopes of lead are as decay products ofradon. Specific consideration is given here to studies of the absorption of lead administered inthat form, and to studies using other ionic forms (e.g. nitrate) that were designed toinvestigate the absorption of radon decay products from the respiratory tract. Dose
coefficients for isotopes of lead inhaled as radon decay products are given in the radon
section, where factors such as the relevant aerosol size distribution are addressed. Otherwise,
exposures to radioisotopes of lead occur most often as decay products associated with intakesof uranium, thorium or radium.
(a) Gases and vapours
Tetra ethyl lead (TEL)(392) Heard et al. (1979) followed the biokinetics of 203Pb for about a week after
inhalation of 203Pb-labelled tetra-methyl lead (TEL) vapour by four healthy male volunteers.
Initial deposition averaged 37% of the inhaled vapour. There was rapid uptake of 203Pb fromthe lungs, with the first blood samples taken 3 minutes after intake indicating ~10% of thedeposit in the cells and ~30% in the plasma; and hence an absorption rate greater than 100 d–
1. The systemic behaviour was different from that of inorganic lead. Loss from blood wasmuch faster: concentrations in both fractions fell by two orders of magnitude in the first 10
hours. At 1 hour >50% of 203Pb deposited from inhalation was present in the liver, remaining
fairly constant during the remaining 6 days of observation. About 20% of the 203Pb-TEL
deposited was lost by exhalation within 48 hours. These results indicate about 40% depositionin the respiratory tract with Type F absorption for TEL.
Tetra methyl lead (TML)(393) Three of the subjects in the study of TEL above inhaled 203Pb-labelled tetra-methyl
lead (TML) in separate studies (Heard et al., 1979). Initial deposition averaged 51% of theinhaled vapour. The behaviour of 203Pb inhaled as TML was similar to that for TEL, with
rapid uptake of 203Pb from the lungs, except that initially more 203Pb was in the cells than in
the plasma. About 40% of the 203Pb-TEL deposited was lost by exhalation within 48 hours.
These results indicate about 50% deposition in the respiratory tract with Type F absorption
for TEL.
(394) However, although specific parameter values for TEL and TML based on in vivo
data could be assessed, they are not adopted here, because inhalation exposure to it is sounlikely. Furthermore the systemic behaviour of lead inhaled in these forms differs from thatof the model adopted here. The information is, however, useful for comparison with the
behaviour of lead inhaled in ionic form, which is absorbed from the lungs much more slowly
than lead inhaled in these organic forms.
(b) Lead as a decay product of radon(395) In this section studies are considered in which 212Pb (half-life 11 hours) formed fromdecay of 220Rn (half-life 56 seconds) and 216Po (half-life 0.15 seconds), or 214Pb (half-life 27
minutes) formed from decay of 222Rn (half-life 3.8 days), and 218Po (half-life 3.1 minutes)
was inhaled directly, while still airborne. For decay schemes, see the thorium and uranium
sections. Studies in which lead ions were inhaled as nitrate or chloride, or in which lead ions137

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5332
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5334
5335
5336
5337
5338
5339
5340
5341
5342
5343
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5346
5347
5348
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5350
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5353
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5357
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5360
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5363
5364

(either formed from decay of 220Rn and 216Po, or as nitrate) were administered to therespiratory tract in a liquid medium, which are also relevant to lead as a decay product ofradon, are considered below in the section on particulate forms.
Lead as an unattached decay product of radon(396) Booker et al. (1969) followed lung retention, blood concentration and fecal excretionof 212Pb for up to 3 d after inhalation (by mouth) of unattached 212Pb (vapour, formed fromdecay of 220Rn/216Po) by one volunteer. In a complementary experiment, the amount of 212Pb
in blood was measured at times up to 2 d after intravenous injection of 212Pb into the same
volunteer. Of the initial deposit in the respiratory tract, 37% was recovered in faeces during
the first 3 d, which the authors attributed to high deposition in the upper airways. Overall,clearance from the chest occurred with a half-time of about 10 hours.
(397) Detailed analyses, of this and other studies, were carried out here (i.e. by the Task
Groups), to estimate absorption parameter values appropriate for short-lived radon progeny.
The studies by James et al. (1977) and Greenhalgh et al. (1979, 1982) outlined below, whichwere designed to investigate the early clearance of lead ions deposited in the lungs, showed a
rapid phase: about 10–40% absorbed with a half-time of about 15 minutes, and evidence thatsome of the slow phase was due to binding. Specific consideration was therefore given here
to the rapid absorption phase and the bound state. For this experiment, absorption parametervalues were assessed from the lung, blood and fecal data published by Booker et al. (1969)
using a subject-specific systemic model, and assuming an absorption model with a rapid
dissolution rate (sr) of 67 d–1 (half-time 15 minutes) and slow dissolution (ss) and uptake (sb)rates of 1.7 d–1 (10-hour half-time). Other parameter values were assessed to be fr = 0.36 and
fb = 0.82, which gives rapid absorption of about 6% of the initial deposit [fr*(1–fb)]. Activity
deposited in the upper respiratory tract retained in particulate form would mainly clear by
mucociliary action to faeces, whereas activity retained in the bound state would not. Thispotentially enables a distinction to be made between the two pathways (provided sr, and hencetransfer to the bound state, is fast compared to particle transport). The faecal measurement
was lower than the predicted value, even with the high bound fraction estimated, and suggeststhat sr is > 67 d–1. However, because the result was only for one volunteer and because ofmeasurement uncertainties, it was judged here that it did not provide a better basis for
estimating sr than the information on which the value of 67 d–1 was based.
(398) Butterweck et al. (2001, 2002) carried out volunteer experiments to determine theabsorption rate of unattached radon progeny. Twenty-one volunteers were exposed in a radon
chamber with well-controlled aerosol and radon progeny conditions. The aerosol was
predominantly unattached radon progeny. Eleven volunteers inhaled by mouth and seven by
nose. Measurements were made of radon gas and progeny (214Pb and 214Bi) in blood samples
taken at the end of a 30-minute exposure (Butterweck et al., 2002). In vivo measurements of
the head and chest were carried out over a 30-minute period, starting approximately 7 minutes
after exposure (Butterweck et al,. 2001). No clearance from the head (other than physicaldecay) was observed over this period, indicating that small fractions of the unattached 214Pb
and 214Bi were absorbed rapidly to blood (sr >> 100 d–1), as measured by the blood sample,
while the rest (fraction fb) was bound to tissues (or stationary mucus). Assuming a rapid
dissolution rate (sr) of 1000 d–1 with fr = 1.0 and an uptake rate from the bound state (sb) of
1.7 d–1, Butterweck et al. (2002) estimated that fb was in the range 0.7–0.85 for radon progeny(without distinguishing between 214Pb and 214Bi). In this study the fraction of the initialdeposit that was rapidly absorbed [fr*(1–fb)] was in the range 0.15–0.3, which is more thanobserved in the study by Booker et al. (1969) (see above). These data were re-evaluated here138

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5374
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5378
5379
5380
5381
5382
5383
5384
5385
5386
5387
5388
5389
5390
5391
5392
5393
5394
5395
5396
5397
5398
5399
5400
5401
5402
5403
5404
5405
5406
5407
5408
5409
5410
5411
5412

using a systemic model based on the ICRP Publication 67 model for lead (ICRP, 1993) but
modified to take account of the early rapid exchange between plasma and extravascular fluid.
Assuming sr = 1000 d-1 with fr=1 they estimated fb was ~0.7 for lead. The longer-duration
measurements made by Booker et al. (1969) are consistent with assignment to Type F.
(399) Bianco et al. (1974) followed chest retention and blood concentration of 212Pb for up
to 2 d after inhalation by dogs (via endotracheal tube) of unattached 212Pb (formed from decayof 220Rn/216Po, effective diffusion diameter of about 11 nm). Fitting a single exponentialfunction to the chest data (after correction for 212Pb in blood) gave an average biological halftime for lung clearance of about 12 hours with values in the range 7 – 20 hours. The
corresponding absorption half-time would be greater, because no correction was made for
mucociliary clearance. However, some would have occurred before the first chest
measurement took place, and similarly there could have been some rapid absorption that was
not observed. There is insufficient information in the paper for more detailed analysis.
Lead as a radon decay product attached to ambient aerosols(400) Booker et al. (1969) followed blood concentration, urinary and fecal excretion of212
Pb in two volunteers for up to 3 d after inhalation (by mouth) of an aerosol formed bymixing 212Pb (formed from decay of 220Rn/216Po) with particles (condensation nuclei, mainly
0.05–5 µm diameter). In complementary experiments, the amount of 212Pb in blood wasmeasured at times up to 2 d after intravenous injection of 212Pb into the same volunteers. Of
the initial respiratory tract deposit (IRTD), only 2–3% was recovered in faeces during the first
3 d, which the authors attributed to low deposition in the upper airways. Overall clearance
from the chest was deduced from the blood measurements to occur with a half-time of about
10 hours. The authors noted that this was similar to that observed following inhalation of
unattached 212Pb (see above), even though it was expected that for 212Pb attached to particles
there was relatively greater deposition in the lower than in the upper respiratory tract, andsuggesting similar rates of absorption to blood in both cases.
(401) Hursh et al. (1969) followed lung retention, blood concentration, urinary and fecal
excretion of 212Pb in ten volunteers for up to 3 d after inhalation (by mouth) of an aerosol
formed by mixing 212Pb (formed from decay of 220Rn/216Po) with natural room aerosol. On
average about 3% IRTD was excreted in urine in the first 24 hours, and total fecal excretion(in 24 – 76 hours) was about 3% IRTD. The authors estimated that on average clearance of212
Pb from lungs to systemic tissues occurred with a half time of 6.5 hours, although they
inferred (from detailed measurements of urinary excretion) that some lead was absorbed
promptly from the lungs. They noted that 212Pb in blood and systemic tissues made asignificant contribution to uncertainty in the lung measurements, but complementary
intravenous injection experiments, which would have enabled direct correction to be made,were not carried out.
(402) Hursh and Mercer (1970) followed lung retention, blood concentration, and urinary
and fecal excretion of 212Pb in four volunteers for up to 3 d after inhalation (by mouth) of anaerosol formed by mixing 212Pb (formed from decay of 220Rn/216Po) with natural room
aerosol. In complementary experiments, the amount of 212Pb in blood was measured at times
up to 2 d after intravenous injection of 212Pb into the same volunteers. On average about 2%
IRTD was excreted in urine in the first 24 hours and total fecal excretion (in 34 – 50 hours)
was 0.35% IRTD: the authors inferred that the latter suggested low deposition in ciliatedairways. They noted that in two subjects the blood lead appeared to increase more rapidly
than for the other two, and that this suggested that 212Pb inhaled as freshly generated 212Pb ofvery small diameter may be more readily absorbed from the lung parenchyma to blood than139

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an aged aerosol associated with larger diameter particles. However, the authors noted that“the determination is not sufficiently precise to establish this relationship.” They estimatedthat, on average, clearance of 212Pb from lungs to systemic tissues occurred with a half time of
10.5 to 11.5 hours, after correcting for activity outside the lungs.
(403) Singh et al. (1986) reported that concentrations of 210Pb (half-life 22 years) in thelungs of uranium miners obtained at autopsy were several times higher than concentrations of
238
U, 234U or 230Th. This indicated that there were sources of intake of 210Pb in addition touranium ore dust. The authors suggested several possibilities, one of which was inhalation of210
Pb present in the mine air but not associated with ore dust. If this originated from radon in
the mine air it suggests that it was retained in the lungs in a relatively insoluble (Type M or S)
form.
(404) Marsh and Birchall (1999) re-evaluated the published data from experiments inwhich volunteers inhaled 212Pb attached to condensation nuclei or to ‘natural’ particles inroom air (Booker et al., 1969; Hursh et al., 1969; Hursh and Mercer, 1970) to estimate anabsorption half-time for lead, assuming a single component. The best estimate obtained was
10 hours with a 95% confidence interval of ±2 hours, which gave an absorption rate of about
1.7 d–1. A more detailed analysis of these and other studies was carried out here to estimate
absorption parameter values appropriate for short-lived radon progeny, giving specificconsideration to the rapid absorption phase (see paragraph above on lead as an unattacheddecay product of radon). The published data from experiments in which volunteers inhaled212
Pb attached to condensation nuclei were re-evaluated with a two-component model.
Assuming sr = 67 d-1 (half-time 15 min) values of fr and ss of 0.06 and 1.4 d-1 (half-time 12 h)
respectively were estimated. However, the information did not permit assessment of fb as forunattached 212Pb (see above), because there was low deposition in the upper respiratory tract(and for Booker et al., 1969, no direct measurements of activity in the lungs).
(405) Based on these studies and those below on ionic lead, lead nitrate and lead oxide,bound state parameter values for lead of fb = 0.5 and sb = 1.7 d–1 were chosen here (seebelow). For the studies of radon as a decay product above, and ionic lead below, specificparameter values were estimated of about fr = 0.3, sr = 100 d–1, ss = 1.7 d–1, fb = 0.8 andsb = 1.7 d–1, i.e. a somewhat higher value of fb. Note that (neglecting particle transport) the
fraction of the initial deposit in the respiratory that is absorbed into blood in the rapid phase isgiven by fr*(1 – fb), thus these parameter values are consistent with rapid absorption of 0.3*(1– 0.8) = 0.06. A similar fractional rapid absorption would be obtained with fb = 0.5 and fr =0.12. Absorption parameter values: fr = 0.1, sr = 100 d–1, ss = 1.7 d–1, fb = 0.5 and sb = 1.7 d–1(consistent with assignment to default Type F) are used here for lead as a short-lived decay
product of radon.
(c) Particulate aerosols
Ionic lead(406) Greenhalgh et al. (1978, 1979) investigated the absorption of lead ions (203Pb or
214Pb) instilled into the bronchi of rabbits or rats in different media. In rabbits, the averageamounts in blood at 20 and 42 minutes after instillation (estimated at about 4% and 7%
respectively of the amount instilled) were similar, whether instilled in lead nitrate solution or
in fresh rat mucus (both isotopes), or in isotonic saline (203Pb). The authors inferred thatabout 10% of instilled lead was absorbed in a rapid phase with a half-time of about 10
minutes. In rats, systemic absorption of 203Pb at 30 minutes after instillation in water,
isotonic saline or hypertonic saline was similar, averaging 42% of the amount instilled, but
140

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higher than in rabbits (~13%). It was somewhat higher when instilled as nitrate (53%), and in
0.1N HCl (61%).
(407) Greenhalgh et al. (1982) investigated the rapid clearance phase of radon decay
products by comparing the biokinetics of ionic 212Pb with those of insoluble radiolabelled
particles (88Y-labelled fused aluminosilicate, FAP) instilled together onto the nasal mucosa ofrats. The 88Y-FAP acted as a tracer for deposition and mucociliary clearance. The suspension
was prepared by collecting 216Po ions from the decay of 220Rn in a chamber onto an electrode,and transferring the 212Pb formed to distilled water: a suspension of the 88Y-FAP in water wasallowed to dry out, and the 212Pb solution was added to the container. Activity retained in thehead, and blood concentration, were followed for 100 minutes. By the end of the experiment
about 8% of the 212Pb had been absorbed (rate about 66 d–1). (Thus rapid absorption of theinitial deposit [fr*(1–fb)] was about 8%.) Nevertheless, the fraction of the initial deposit
remaining in the nose was greater for 212Pb (~40%) than for the particles (~30%). The authors
concluded that some of the 212Pb was retained by binding either to static mucus or epithelial
tissue, and developed a two phase (sol and gel) model of mucociliary clearance to explain the
results. Analysis carried out here, assuming slow dissolution (ss) and uptake (sb) rates of 1.7
d–1 (10-hour half-time, see paragraph above on lead as an unattached decay product of radon)gave absorption parameter values of fr = 0.35, sr = 60 d–1 (half-time 17 minutes), and fb = 0.7.
Lead nitrate (Pb(NO3)2)(408) James et al. (1977) followed the biokinetics of 212Pb for up to 100 minutes after
instillation of 212Pb-nitrate into the trachea or bronchioles of rabbits. (The solution was
prepared by collecting 216Po ions from the decay of 220Rn in a chamber onto an electrode, andtransferring the 212Pb formed to distilled water containing stable lead nitrate carrier.) From
both sites approximately 20% of deposited 212Pb was absorbed to blood with a half-time ofabout 4 minutes (250 d–1), and the remainder with a half-time estimated at about 9 h (1.8 d–1).
Insoluble radiolabelled particles were instilled simultaneously into the bronchioles of one
rabbit to act as a tracer for mucus. It was found that despite absorption to blood, the 212Pb
cleared more slowly than the particles, and it was inferred that this indicated slow diffusion of212
Pb through the epithelium (i.e. that some binding occurs). It was reported that by the endof the experiment (2 hours after instillation) more of the 212Pb remaining in the lungs was
associated with mucus than with epithelium.
(409) Chamberlain et al. (1978) administered to four volunteers an aerosol of 203Pblabelled nitrate (AMAD in the range 0.4–0.8 µm), formed by adding nitrogen to the flame
produced by burning 203Pb-labelled tetra-ethyl lead in propane. Measurements of 203Pb in thechest, blood and excreta were made for about 4 days. Complementary measurements werealso made of 203Pb in the legs, to correct lung measurements for systemic 203Pb, based on the
results of similar measurements made after intravenous injection of 203Pb. Lung retention was
represented by a three-component exponential function with half-times of 1.0 hours (26%);
2.2 hours (33%); and 10 hours (41%) (rates of 17, 7.6 and 1.7 d–1 respectively). Clearance
was almost entirely by systemic uptake: only a small percentage of the initial lung deposit(ILD) was cleared by mucociliary action and swallowed. Chamberlain et al. (1978) noted thatlead nitrate was far more soluble in vitro than indicated by the lung measurements, andsuggested that the mechanism for transferring lead from lung fluid to blood is a relatively
slow process, which determines the overall transfer rate.
(410) Ballou et al. (1986) measured lung retention and tissue distribution of 232U, 228Th,
224
Ra, 212Pb, 212Bi and 208Tl at 24 hours after intratracheal instillation into rats of 232U nitratewith its decay products. (For further information, see the uranium inhalation section.) For
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212

Pb, on average 2.1% ILD was measured in the lungs at 1 day. Correcting for the physicaldecay of 212Pb gives retention of 10% ILD at 1 day.
(411) Moody et al. (1994b); Moody and Stradling, 1992) measured the tissue distributionof 228Th, 212Pb, 212Bi and 208Tl, at times from 6 hours to 7 days after intratracheal instillation
into rats of a nitrate solution of 228Th in equilibrium with its decay products. (Radon-220 is aprecursor of 212Pb, but it is unlikely that a significant amount was lost from solution before
deposition in the lungs, because of its short half life of 56 seconds. Its average half distance ofdiffusion in water was estimated to be 50 µm by Ballou and Hursh, 1972.) For 212Pb, on
average 8.4% of the initial lung deposit (ILD) was measured in the lungs at 6 hours and 1.2%
ILD at 1 day: clearance was much faster than that of the parent 228Th. Correcting for thephysical decay of 212Pb gives retention of 12.5% ILD at 6 hours and 5.6% ILD at 1 day. Fromthese results it was assessed here, assuming either (i) that the retained lead was in particulate
form, i.e. a slow dissolution (ss) rate of 1.7 d–1 with no bound state (fb=0) or (ii) that theretained lead was in the bound state with an uptake rate (sb) of 1.7 d–1 with no slow
dissolution (fr=1) (see paragraphs above on lead as a decay product of radon), that sr was ~50
d–1 (half-time ~20 min) with fr ~0.75 or fb ~0.25 respectively, i.e. about 75% cleared rapidly
in either case. Later measurements were not included because of possible significant
contributions to measured 212Pb from decay of higher members of the chain.
(412) Based on these studies and others, bound state parameter values for lead of fb = 0.5
and sb = 1.7 d–1 were chosen (see below). It is noted that (neglecting particle transport) the
fraction of the initial deposit in the respiratory that is absorbed into blood in the rapid phase isgiven by fr *(1 – fb), which for fb = 0.5, gives fr *(0.5). For the study in which lead nitrate wereinhaled by human volunteers (Chamberlain et al., 1978), ~50% ILD was cleared rapidly(components with half times less than 3 hours), suggesting a value for fr of ~1.0. Specificparameter values derived for lead nitrate would be close to those for Type F (including thebound state parameters for lead), and therefore lead nitrate is assigned here to Type F.
Lead chloride (PbCl2)(413) Morrow et al. (1980) followed lung retention and blood concentration of 203Pb ineight volunteers for up to 4 d after inhalation (by mouth) of an aerosol formed by nebulising asodium chloride vector solution to which carrier-free 203PbCl2 was added, giving an AMAD
of ~0.25 µm. Lung retention was represented by a two-component exponential function withon average (after correction for systemic 203Pb and physical decay) 7% clearing at a rate of
0.023 min–1 (33 d–1, half-time 30 minutes) and 93% at a rate of 0.00088 min–1 (1.3 d–1, halftime 13 hours). The corresponding absorption rates would be lower, because of particle
transport to the alimentary tract. However, at this aerosol size deposition in the upper
respiratory tract would have been relatively low, and so the contribution would be small, atleast to the slow phase. The authors noted that the blood data suggested that the rapid phase
could be due to absorption rather than mucociliary clearance. Some mucociliary clearance andsome rapid absorption would have occurred before the first chest measurement took place,shortly after aerosol administration. Without fecal clearance measurements, estimates of
specific absorption parameter values could not be made here: the results are consistent withassignment to Type F.
Lead hydroxide (Pb(OH)2)(414) Morrow et al. (1980) followed lung retention and blood concentration of 203Pb innine volunteers for up to 4 d after inhalation (by mouth) of a Pb(OH)2 - NaCl aerosol formedby nebulising a sodium chloride vector solution to which carrier-free 203PbCl2, stable lead
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chloride and sodium hydroxide were added, giving an AMAD of ~0.25 µm. Lung retention
was represented by a two-component exponential function with on average (after correction
for systemic 203Pb and physical decay) 12% clearing at a rate of 0.012 min–1 (17 d–1, half-time
60 minutes) and 88% at a rate of 0.00081 min–1 (1.2 d–1, half-time 14 hours). The authors
noted that the results were not significantly different from those obtained with carrier-freelead chloride (see above) despite differences in chemical form and mass. As for the chloride,
estimates of specific absorption parameter values could not be made: the results are consistent
with assignment to Type F.
(415) Stradling et al. (2005; Moody et al., 1994a) measured the tissue distribution of 228Th,
212
Pb, 212Bi and 208Tl, at times from 1 to 168 days after intratracheal instillation into rats of asuspension of 228Th hydroxide in equilibrium with its decay products. For 212Pb, on average
2.7% ILD was measured in the lungs at 1 day, when administered with a low mass (50 pg) of
thorium, (5% ILD when administered with a high mass, 6.5 µg, of thorium). Clearance wasmuch faster than that of the parent 228Th. Correcting for the physical decay of 212Pb gives
retention of 13% ILD at 1 day. From this result it was assessed here that sr was greater than 2
d–1 (half-time ~8 hours). Alternatively, assuming fr = 1, and sr = 100 d–1 gave fb = 0.8. Latermeasurements were not included because of possible significant contributions to measured
212
Pb from decay of higher members of the chain. There was insufficient information toquantify a slower phase as seen in other studies of soluble forms of lead: its presence would
give a higher value for sr. The results are consistent with assignment to Type F, to which leadhydroxide is assigned.
Lead oxide (PbO and Pb3O4)(416) Rendall et al. (1975) measured lead levels in blood (only) of baboons that inhaled
red lead oxide (Pb3O4): either as a “coarse” (mass median diameter, MMD, 6 µm) or “fine”(MMD 2 µm) aerosol at similar mass concentrations. There is insufficient information toassess absorption parameter values, but blood levels were higher following exposure to coarse
than to fine dust. Since it is likely that for the coarse dust deposition in the upper respiratory
tract (URT) was higher and deposition in the lungs lower than for the fine dust, the results
suggest that there was rapid absorption from the URT and/or the alimentary tract.
(417) Boudene et al. (1977) measured tissue distribution and excretion in rats for 6 days
following inhalation (whole body) of an aerosol formed by passing nebulised gasoline
labelled with organic 210Pb with air through a tube furnace at 600°C. Lung clearance was
rapid, reducing to 11% ILD at 24 hours and 1% ILD at 6 days. There is detailed informationon the biokinetics (nine time points within the first day) but large uncertainties on thedeposition pattern (extrathoracic and pelt). From the results, parameter values assessed here,
assuming that the lead which was not cleared in the rapid phase was retained in the boundstate (fr =1) were sr ~5 d–1 (half-time ~3 hours); fb ~0.2 and sb ~0.5 d–1 (half-time ~33 hours),
giving assignment to Type F.
(418) Chamberlain et al. (1978) administered to six volunteers an aerosol of 203Pb-labelledoxide (AMAD in the range 0.4–0.8 µm), formed by eliminating nitrogen from the flame
produced by burning 203Pb-labelled tetra-ethyl lead in propane. Measurements of 203Pb in thechest, blood and excreta were made for about 4 days. Complementary measurements werealso made of 203Pb in the legs, to correct lung measurements for systemic 203Pb, based on the
results of similar measurements made after intravenous injection of 203Pb. Lung retention was
represented by a four-component exponential function with half-times of 0.5 hours (25%); 2.9
hours (32%); 9.8 hours (25%) and 38 hours (18%) (rates of 33, 5.7, 1.7 and 0.4 d–1
respectively). Clearance was almost entirely by systemic uptake: only a small percentage of143

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the initial lung deposit (ILD) was cleared by mucociliary action and swallowed. Chamberlain
et al. (1978) noted that (in contrast to nitrate and motor exhaust aerosols) the lead oxide wasless soluble in vitro than indicated by the lung measurements, and suggested that this might
be because of efficient fluid flow in the lungs.
(419) Rhoads and Sanders (1985) followed the biokinetics of lead in rats for 91 days after
inhalation of non-radioactive PbO. Lung retention was represented by a two-component
exponential function with half-times of 1 day (93%) and 89 days (7%), consistent withassignment to Type F.
(420) Lung retention of lead oxide inhaled by human volunteers was similar to that of leadnitrate (Chamberlain et al., 1978), and therefore specific parameter values derived from themwould also be close to those for Type F (including the bound state parameters for lead), andtherefore lead oxide is assigned here to Type F.
Lead difluoride (PbF2)(421) Stradling et al. (2005; Moody et al., 1994a) measured the tissue distribution of 228Th,
212
Pb, 212Bi and 208Tl, at times from 1 to 168 days after intratracheal instillation into rats of asuspension of 228Th fluoride in equilibrium with its decay products. For 212Pb, on average
6.0% ILD was measured in the lungs at 1 day, when administered with a low mass (60 pg) of
thorium. Correcting for the physical decay of 212Pb gives retention of 28% ILD at 1 day.
Clearance was faster than that of the parent 228Th. From this result it was assessed here that sr
was at least 1 d–1 (half-time ~8 hours). Later measurements were not included because of
possible significant contributions to measured 212Pb from decay of higher members of thechain. There was insufficient information to quantify a slower phase as seen in other studies
of soluble forms of lead: its presence would give a higher value for sr. (However, whenadministered with a high mass, 6.5 µg, of thorium, 18% ILD of 212Pb was measured in thelungs at 1 day. Correcting for the physical decay of 212Pb gives retention of ~80% ILD at 1
day, similar to that of the parent thorium.) The results indicate Type F behaviour and lead
difluoride is assigned to Type F.
Lead in fresh or age-aggregated motor exhaust (including lead dibromide, PbBr2)(422) Although mainly related to environmental, rather than occupational, exposure,
information relating to lead in motor exhaust and tobacco smoke is included here forcompleteness.
(423) Chamberlain et al. (1975, 1978) administered various aerosols derived from 203Pblabelled motor exhaust to several volunteers. Measurements of 203Pb in the chest, blood andexcreta were made for up to about 4 days. Complementary measurements were also made of203
Pb in the legs, to correct lung measurements for systemic 203Pb, based on the results ofsimilar measurements made after intravenous injection of 203Pb. (Absorption from thealimentary tract following ingestion of exhaust particles collected on filters was also
determined.) In most cases, patterns of lung clearance and systemic uptake were similar to
those found by these authors for lead inhaled as nitrate or oxide (see above), often in the same
volunteers. For fresh motor exhaust, Chamberlain et al. (1978) represented lung retention by athree-component exponential function with half-times of 1.2 hours (27%); 2.3 hours (39%);
and 8.1 hours (34%) (rates of 14, 7.2 and 2.1 d–1 respectively). Clearance was almost entirely
by systemic uptake: only a small fraction of the ILD was cleared by mucociliary action andswallowed. For aged exhaust (stored and in some cases exposed to ultraviolet light) a fourthcomponent was needed: about 10%-15% was retained with a half-time of 40-220 hours.
(Chamberlain et al., 1975, reported only that most of the 203Pb in the lungs was retained with
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a half-time of about 6 hours, and the rest cleared more slowly.) Most studies of thecomposition of exhaust lead (e.g. Habibi 1973) have identified complex mixtures of leadoxides, halides and ammonium salts, together with sulphates and carbonaceous material. Thissuggests that Type F behaviour may be characteristic of many lead compounds other thanthose for which specific information is available. In particular, since lead dibromide was animportant constituent of lead in motor exhaust, it suggests that, like lead chloride, it should be
assigned to Type F.
Lead-210 in cigarette smoke tar(424) A brief summary is given here: for further information see the polonium section.
Lead-210 and its decay product, 210Pb, are inhaled in cigarette smoke (Desideri et al., 2007).
Martell (1974) reported that 210Pb concentrates in resinous material in tobacco leaves,forming insoluble particles during combustion. Cohen et al. (1979) measured 210Po
concentrations in the tracheobronchial tree and lung parenchyma in autopsy tissues fromsmokers and non-smokers, and attributed differences to the retention of insoluble particles
containing 210Pb/210Po in cigarette smoke. Cohen et al. (1985) measured 210Po in the lungs ofrats after exposure to cigarette smoke enriched in 210Pb/210Po: results indicate Type M or S
behaviour for both the 210Pb and 210Po.
Mineral dust(425) A potentially important source of intake of 210Pb in particulate aerosols arises fromairborne mineral dusts containing the natural long-lived parent. In this case the absorption rate
will probably be determined by the dissolution rate of the mineral matrix in lung fluids.
Measurements have been made of the dissolution in simulated lung fluid of samples of coal
fly ash (Kalkwarf et al., 1984) and condensate from calcining phosphate rock dust (Kalkwarf
and Jackson, 1984) for 60 days. By this time the amounts of 210Pb dissolved were <0.2% and<5% respectively, indicating assignment to Type S in both cases.
Uranium ore dust(426) Duport et al. (1991) measured the dissolution in simulated lung fluid of long lived
radionuclides in uranium ore dust from Canadian mines. (For further information see theuranium section relating to uranium ore dust and to decay products of uranium formed in the
respiratory tract). For high grade ore, measurements were made for up to 60 days. Results
were presented as undissolved fractions as functions of time, and showed two components,
which were expressed as Class D (rapid) and Class Y (slow) fractions. For 210Pb the rapidly
dissolved fraction was 0.28. HRTM parameter values fitted to the 210Pb data by Marsh et al.
(2011) were: fr = 0.26, sr = 3.9 d–1 and ss = 0.001 d–1, indicating assignment to Type M. For
210
Pb, no effects of size were observed in total dissolution over 40 days for particles in size
ranges 7–10, 3–7, 1–3 and <1 µm. For low grade and medium grade ores, measurements weremade for 12 days, but only on samples of relatively coarse dust, the smallest fraction being<37 µm. For 210Pb, rapidly dissolved fractions were lower, <0.01, indicating assignment toType S.
Thorium dioxide(427) Hodgson et al. (2000, 2003) measured the tissue distribution of 228Th, 212Pb, 212Bi
and 208Tl, at times from 1 to 168 days after intratracheal instillation into rats of suspensions of
232
Th dioxide enriched with 228Th, in equilibrium with its decay products, with geometricdiameters of about 0.4 and 2 µm. (For further information, see the thorium inhalation
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section.) There was little absorption of the thorium itself, consistent with assignment to Type
S. The activity of 212Pb in the lungs was about 50% and 80% of that of the thorium at 1 day
for the 0.4 and 2 µm particles respectively, and 25% and 70% at later times. The lower
concentrations of 212Pb were attributed to diffusion of 220Rn (thoron) and recoil of theprogeny from alpha particle decay.
Decay products of lead formed in the respiratory tract(428) The general approach to treatment of decay products formed in the respiratory tract
is described in Part 1, Section 3.2.3. In summary, it is expected that generally the rate at
which a particle dissociates is determined by its matrix, and hence the physico-chemical formof the inhaled material. It is recognised that nuclei formed by alpha decay within a particle
matrix may be expelled from it into the surrounding medium by recoil, but to implement thisroutinely would add greatly to the complexity of calculations. It is expected that the behaviourof soluble (e.g. Type F) material in the respiratory tract would depend on its elemental form,
i.e. that of the decay product. Nevertheless, for simplicity, in this series of documents theabsorption parameter values of the parent are, by default, applied to all members of the decay
chain formed in the respiratory tract. Exceptions are made for noble gases formed as decay
products, which are assumed to escape from the body directly, at a rate of 100 d–1, in addition
to other routes of removal.
(429) For decay schemes of lead isotopes in the natural decay series, including 214Pb, 212Pb
and 210Pb, see the uranium and thorium sections. Studies specifically comparing the
behaviour of lead with that of its decay products (bismuth and thallium isotopes) aresummarised here. For further information, see the bismuth inhalation section.
(430) Drew (1971) reported that the tissue distributions of 212Pb (half-life 11 hours) and212
Bi (half-life 61 minutes) activities were similar in rats following exposure to 220Rn (thoron)
and its decay products for 2 days. However, the exposure situation was complex, because the212
Pb and 212Bi in tissues originated from inhalation of 220Rn, and its decay within the body,inhalation of 212Pb and 212Bi, and also their ingestion from food and preening of fur. It istherefore difficult to estimate how much of the 212Bi originated from decay of 212Pb in thelungs. Furthermore, 212Bi would have grown in rapidly between dissection of the animals andmeasurements of activities in tissues. Thus the activities of 212Bi present in vivo may havebeen significantly lower than those measured.
(431) As noted above, measurements have been made of the tissue distributions of 212Pb
and its decay products, 212Bi and 208Tl, following administration to rats of 228Th in various
chemical forms (nitrate, hydroxide, fluoride, dioxide), in equilibrium with its decay products.
In all these studies the distributions of 212Bi and 208Tl were similar to each other and those of
the parent 212Pb. Because their physical half-lives are so short (61 minutes and 3 minutes
respectively) measurements made at 6 hours onwards would be mainly of activity formed
from decay of 212Pb within the body, rather than from intake of 212Bi (or 208Tl). The similar
distributions of 212Bi (and 208Tl) to those of 212Pb might suggest that there was not rapid
movement of 212Bi from the site (e.g. the lungs) in which it was formed by decay of 212Pb.
However, 212Bi (and 208Tl) would have grown in rapidly between dissection of the animals
and measurements of activities in tissues. Without detailed information (which is notavailable) about the time which elapsed between dissection of the animals and measurements,
it is not possible to correct for this ingrowth and hence estimate the absorption rates of thebismuth or thallium formed as a decay products in the lungs. However, since the half-life of208
Tl is so short (as is that of 207Tl present in the 235U decay series, 5 minutes), the absorption
rate of thallium would have to be very high to influence dose assessments.
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5796

(432) As described above, Butterweck et al. (2001, 2002) measured radon gas, 214Pb and214
Bi in blood samples taken from volunteers at the end of a 30-minute inhalation exposure tounattached radon progeny. In vivo measurements of the head and chest were also carried out.
Assuming a rapid dissolution rate (sr) of 1000 d–1 with fr=1 and an uptake rate from the boundstate (sb) of 1.7 d–1, Butterweck et al. (2002) estimated that the rapid absorption of the initialdeposit is in the range 0.15–0.3 and the remaining fraction is bound with fb in the range 0.7–
0.85, for “radon progeny” (without distinguishing between 214Pb and 214Bi). However,
Butterweck et al. (2002) also estimated “absorption rates” for 214Pb and 214Bi from theiractivities in the blood sample and the estimated respiratory tract deposition, assuming thatabsorption from respiratory tract to blood could be represented by a single rate constant (sr)i.e. fr=1 and fb=0, although this model seems inconsistent with the in vivo measurements.
They obtained absorption half-times of ~60 minutes for 214Pb and ~25 minutes for 214Bi,
suggesting that there was greater absorption of 214Bi than of 214Pb by the end of the exposure
when the blood sample was taken.
(433) As noted above, Singh et al. (1986) measured concentrations of 210Pb (half-life 22
years) in the lungs of uranium miners obtained at autopsy. In most (six out of eight) cases
several years elapsed between death and analysis, so that, regardless of its concentration in thelungs at death, 210Po would have reached equilibrium with 210Pb. For the other two miners theanalysis was within a few months of death, and the authors inferred that the results indicatedthat the 210Po and 210Pb were in equilibrium at the time of death.
Rapid dissolution rate for lead(434) The absorption of lead from the respiratory tract following deposition in ionic form
has been studied extensively. There have been human volunteer and laboratory animal studiesof the biokinetics of lead inhaled in several ionic forms: as a decay product of radon and as
nitrate, chloride, hydroxide, fluoride and oxide. There have also been laboratory animalstudies in which solutions of ionic lead were instilled onto the nasal and bronchial epithelium
to study the absorption of lead in more detail. Most of these show a similar pattern. As notedby Morrow et al. (1980), where absorption from the respiratory tract to blood has been
represented by a single overall absorption rate, half-times of about 10 hours were obtained forseveral different forms of lead. For some inhalation studies, the duration of exposure anddelay before the first measurement mean that a minor rapid component (time scale ofminutes) would not have been observed. However, in studies with sufficient data, twocomponents are generally observed, a rapid phase, with between about 10% and 75% clearing
with a half-time between a few minutes and an hour (rate between about 20 and 200 d–1: therest with a half-time of about 10 hours (rate about 1.7 d–1). Exceptions are the humanvolunteer studies of lead as an unattached decay product of radon (Booker et al., 1969,
Butterweck et al., 2001, 2002): the results indicate a rate for the rapid phase > 100 d–1.
Studies of lead inhaled as a decay product of radon give values of sr of about 100 d–1, which
is applied here to all Type F forms of lead.
Extent of binding of lead to the respiratory tract(435) There is strong evidence for a bound state for lead, on a time scale relevant to its
inhalation as a decay product of radon. As noted above, the absorption of lead from therespiratory tract following deposition in ionic form has been extensively studied. In studies
with sufficient data, two components are generally observed, a rapid phase (10–75% clearing
in less than an hour) and the rest with a half-time of about 10 hours.
(436) This similarity in the half-time associated with slow uptake of lead in several
147

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5803
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5809
5810
5811
5812
5813
5814
5815
5816
5817
5818
5819
5820
5821
5822
5823
5824
5825
5826
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5828
5829
5830
5831
5832
5833
5834
5835
5836
5837
5838
5839
5840
5841
5842
5843
5844

different ionic forms suggests that it is a characteristic of the element rather than determinedby dissociation of the different forms. The slow phase was not observed when lead wasinhaled in organic form (tetra-ethyl or tetra-methyl lead): the rate of uptake observed (~50%
in a few minutes), seems consistent with the size of the molecules. Uptake of inorganic ioniclead was much slower, indicating that some mechanism slows down its uptake to blood.
(437) The question of whether the slow phase of absorption of ionic lead represented
binding to respiratory tract components has been considered for over 30 years. Chamberlain
et al. (1978) noted that lead nitrate was far more soluble in vitro than indicated by the lungmeasurements, and suggested that the mechanism for transferring lead from lung fluid toblood is a relatively slow process, which determines the overall transfer rate.
(438) Hursh and Mercer (1970) complemented their inhalation studies of lead as a radon
decay product (see above) with ultrafiltration experiments (transfer though dialysis
membrane): the 212Pb aerosol was collected electrostatically onto a metal plate, and dispersed
ultrasonically into the liquid medium tested. In distilled water or heparinised plasma less than
1% was ultrafilterable, but this was greatly increased by addition of citrate. The authors
attributed the low fraction without added citrate to binding of lead to the dialysis membrane(distilled water) or proteins (plasma).
(439) Most directly, James et al. (1977) and Greenhalgh et al. (1982) compared the
biokinetics of ionic 212Pb with those of insoluble radiolabelled particles instilled together onto
the bronchiolar epithelium of rabbits or nasal mucosa of rats. Despite some rapid absorption
into blood, the 212Pb cleared more slowly than the particles. The authors concluded that someof the 212Pb was retained by binding either to static mucus or epithelial tissue. However, asimilar clearance half-time has been observed with ionic lead deposited predominantly in thealveolar region (see above, e.g. lead as a radon decay product attached to ambient aerosols),
which does not have a mucus lining, suggesting that there is binding to the epithelium.
(440) For the experiment by Booker et al. (1969) in which a volunteer inhaled unattached212
Pb (see above), absorption parameter values assessed here (assuming an absorption modelwith sr = 67 d–1 and ss = sb= 1.7 d–1) were fr = 0.36 and fb = 0.82. Neglecting the bound state(assuming fb = 0) underestimated lung retention and overestimated fecal excretion. Similarparameter values were assessed here from the results of the experiment by Greenhalgh et al.
(1982). Butterweck et al. (2002) estimated fb to be in the range 0.7–0.85, assuming that fr = 1,
from the results of their experiments in which volunteers inhaled unattached radon decay
products: fb was estimated here to be ~0.7 for lead from these data.
(441) Note that (neglecting particle transport) the fraction of the initial deposit in the
respiratory tract that is absorbed into blood in the rapid phase is given by fr*(1 – fb). For thestudies in which lead nitrate and lead oxide were inhaled by human volunteers (Chamberlain
et al., 1978), about 60% ILD was cleared rapidly (components with half times less than 3
hours). (There was little mucociliary clearance and fecal excretion.) These results suggest alower value of fb than the estimates made for lead as a decay product of radon. Similarly, fb
values of about 0.25 were estimated here for lead nitrate instilled into rats or lead oxide
inhaled by rats based on the data of Moody et al. (1994b) and Boudene et al. (1977)
respectively.
(442) On the basis of all these results, a bound fraction with fb = 0.5 and a rate of uptake sb= 1.7 d–1 is adopted here for lead. There is experimental evidence that lead in soluble form
deposited in the conducting airways is retained in a bound state. It is therefore assumed herethat these bound state parameter values apply throughout the respiratory tract (ET2, BB, bb
and AI regions).

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5845
5846
5847

Table 9-2. Absorption parameter values for inhaled and ingested lead

Inhaled particulate materials
Specific parameter valuesc
Lead as a decay product of radon

Absorption
parameter Absorption
fromavaluesthealimentaryfrsr (d–1) ss (d–1) tract, fAb
0.1

Default parameter valuesd
Absorption
Assigned forms
TypeF
Lead dichloride, dibromide, 1
difluoride,hydroxide,
nitrate,oxide,
allunspecified formse
—
M
0.2
S
Mineral dusts
0.01
Ingested material
All forms
5848
5849
5850
5851
5852
5853
5854
5855
5856
5857
5858
5859
5860
5861
5862
5863
5864
5865
5866
5867
5868
5869
5870
5871
5872
5873
5874
5875
5876
5877

100

1.7

0.02

100

–

0.2

3
3

0.005
0.0001

0.04
0.002

0.2

a

It is assumed that for lead the bound fraction fb is 0.5 with an uptake rate sb = 1.7 d–1, and that this applies
throughout the respiratory tract (ET2, BB, bb and AI regions). The value of sr for Type F forms of lead (100d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
b
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type (or specific value where given) and the fA value for ingested soluble forms of lead (0.2).
c
See text for summary of information on which parameter values are based, and on ranges of parameter values
observed in different studies. For lead as a decay product of radon, specific parameter values are used for
dissolution in the lungs, but a default value of fA (footnote b).
dMaterials (e.g. lead dichloride) are listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see text).
eDefault Type F is recommended for use in the absence of specific information, i.e. if the form is unknown, or
if the form is known but there is no information available on the absorption of that form from the respiratory
tract.

9.2.2. Ingestion(443) Lead absorption has been studied extensively in man and animals (See review in
ICRP, 1993). Factors shown to affect absorption of Pb include ingestion of milk, calcium andiron status, protein deficiency, vitamin D and fasting. Of these, fasting causes the greatest
variation in uptake. For example, James et al. (1985) measured absorption in volunteers given203
Pb acetate in water to be about 0.65 after a 12h fast compared with about 0.04 when takenwith a meal. At 3h after a meal, absorption averaged about 0.16 with a range of 0.05 to 0.5,
and after 5h the average was about 0.45 with a range of 0.3 to 0.65. Individual variation was
also shown by Blake (1976) who measured absorption ranging from 0.1 to 0.7 in ten
volunteers given 203Pb chloride. Heard and Chamberlain (1982) showed that fasting values ofabout 0.4 to 0.5 by giving 203Pb as chloride to volunteers in distilled water were reduced to
0.1 to 0.2 in tea, coffee or beer.
(444) Leggett (1993) suggest in its age-specific kinetic model of lead metabolism inhumans, to assign an f1 value of 0.15 in adults.

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5891
5892
5893
5894
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5896
5897
5898
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5900
5901
5902
5903
5904
5905
5906
5907
5908
5909
5910
5911
5912
5913
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5921
5922
5923
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5925

(445) The Publication 30 (ICRP, 1980) derived an absorption value of 0.2 that was appliedin Publication 67 (ICRP, 1993) to dietary intakes. An fA of 0.2 is used here for direct
ingestion of all forms of lead.
9.2.3. Systemic Distribution, Retention and Excretion
9.2.3.1. Summary of the database(446) Following intravenous administration of radiolead to human subjects, the injected
activity initially cleared from blood at a rate of 1 min-1 or greater (Wells et al., 1975;
Chamberlain et al., 1978). A minimum blood content of about one-third of the injectedamount was reached within 2-3 min, at which time roughly three-fourths of activity in blood
resided in red blood cells (RBC). Increased activity in blood was then seen for 24-48 h as thetracer returned from extravascular spaces and accumulated in RBC (Booker et al., 1969;
Wells et al., 1975; Chamberlain et al., 1978). Within a few hours after injection, 99% or moreof activity in blood was bound in or on RBC (Hursh et al., 1969; Booker et al., 1969; Wells etal., 1975; Chamberlain et al., 1978; Everson and Patterson, 1980; DeSilva, 1981; Manton and
Cook, 1984; Heard and Chamberlain, 1984).
(447) At 1-2 d after introduction of radiolead into adult humans by injection or inhalation,
the blood contained 40-75% (mean 58 ± 12%) of the amount reaching the circulation (Hurshand Suomela, 1968; Booker et al., 1969; Hursh et al., 1969; Wells et al., 1975; Chamberlain
et al., 1978; Morrow et al., 1980; Heard and Chamberlain, 1984). Over the next few weeks,
activity was cleared from blood with a biological half-time on the order of 15-20 days
(Rabinowitz et al., 1973, 1974, 1976; Wells et al., 1975; Heard and Chamberlain, 1984).
(448) Soon after introduction of radiolead into blood plasma, the tracer is largely available
for diffusion into extravascular fluids and filtration by the kidneys (Vander et al., 1977;
Chamberlain et al., 1978; Heard and Chamberlain, 1984). Under steady-state conditions,however, most of the lead in plasma is bound to proteins (Griffin and Matson, 1972).
(449) The liver contained about 10-15% of administered radiolead at 1 d after intravenous
injection into adult humans (Heard and Chamberlain, 1984), baboons (Cohen et al., 1970), or
dogs (Lloyd et al., 1975). Most of the activity deposited in the liver was removed with abiological half-time of a few weeks. Autopsy measurements on chronically exposed adulthumans indicate that the liver typically contains about 2-3% of total-body lead. The blood-toliver concentration ratio in chronically exposed persons typically is about 0.2 (Blanchard andMoore, 1970, 1971; Hamilton et al., 1972; ICRP, 1975; Gross et al., 1975; Barry, 1975,198l).
(450) Part of the loss of lead from the liver can be accounted for by biliary secretion into
the gastrointestinal content, but return of lead from the liver to blood also must be postulated
to explain the limited losses in faeces. Estimates of the contribution of biliary secretion tototal faecal excretion of lead are variable. For example, data of Rabinowitz et al. (1976)
indicate that biliary secretion represents no more than half of all endogenous secretion of lead
into the gastrointestinal tract, while data of Ishihara and Matsushiro (1986) suggest that
hepatic bile is the main route of faecal elimination of absorbed lead from the body.
(451) Results of experimental studies on dogs and rodents indicate that the kidneys
accumulated as much as 15-20% of intravenously injected radiolead within the first 1-2 h,most of the accumulated activity represented filtered lead, and a substantial portion of theearly accumulation was reabsorbed or lost in urine within a few hours (Morgan et al., 1977;
Victery et al., 1979; Keller and Doherty, 1980). In rats, the kidneys contained roughly 10% of
the intravenously injected amount after 1 day but less than 2% after 9 days. In baboons
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5953
5954
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receiving radiolead by intravenous injection, the kidneys contained about 4% of theadministered amount after 1 day, 0.6% after 30 days, and 0.1% after 60 days (Cohen et al.,1970). In dogs receiving 210Pb by intravenous injection, the kidneys contained about 0.5% of
the administered activity at 1 month (Lloyd et al., 1975). Comparison of the decline of renal
and hepatic activity from 1 d to about 2 mo after intravenous administration of radiolead tobaboons (Cohen et al., 1970) indicate that the removal half-time from the kidneys is roughly
half of that from the liver, if each of these organs were treated as a single compartment. Thisagrees with estimates for baboons exposed to lead by daily ingestion over a period of a few
months (Mallon, 1983).
(452) Gradual loss of lead from RBC, liver, kidneys, and other soft tissues over the firstfew weeks can be accounted for by a slow loss in urine and faeces and a continual increase inskeletal lead. Typically, 3-5% of injected or absorbed lead is lost in urine during the first day.
The urinary to faecal excretion ratio is about 2 during days 3-14 after absorption of lead toblood in humans. About 30% of intravenously injected radiolead is removed in urine andfaeces during the first 20 days (Hursh and Suomela, 1968; Hursh et al., 1969; Hursh andMercer, 1970; Booker et al., 1969; Wells et al., 1975; Chamberlain et al., 1978; Heard andChamberlain, 1984).
(453) In baboons (Cohen et al., 1970) and human subjects (Heard and Chamberlain, 1984),
there was evidence of rapid skeletal uptake of about 10-15% of intravenously administeredlead. The skeletal content remained nearly constant over the next 2-3 d and then slowly
increased over an extended period as activity returned from RBC and soft tissues to plasma.
In human subjects the skeleton contained roughly 20% of the injected amount after 20 d.
Autopsy data for persons chronically exposed to environmental lead indicate that the skeletal
content of lead increases throughout life and represents 90% or more of systemic lead by thefifth decade (Tipton and Cook, 1963; Gross et al., 1975; Barry, 1975, 1981; Leggett, 1993).
(454) Skeletal behaviour of lead appears to be qualitatively similar to that of the alkaline
earth elements and quantitatively similar to that of barium or radium, if account is taken of
the slower deposition of lead in the skeleton due to competition from RBC (Hursh, 1973;
Lloyd et al., 1975; Domanski and Trojanowska, 1980; Heard and Chamberlain, 1984). Leadhas been used frequently as a marker of bone growth and osteon formation, and a close
resemblance to calcium has been demonstrated in such studies (Vincent, 1957; Lacroix, 1960;
Scheiman-Tagger and Brodie, 1964; Hong et al., 1968; Yen and Shaw, 1977). Lead isincorporated into the crystalline structure of bone, where it replaces calcium ions (MacDonald
et al., 1951; Verbeeck et al., 1981; Miyake et al., 1986).
(455) Autoradiographs of bone sections from baboons injected with 210Pb indicate that a
portion of skeletal activity remains near bone surfaces at 1 to 2 months after administration,
as appears to be the case for radium and barium. Studies on human subjects indicate that the
distribution of lead in bone may be skewed toward bone surfaces for at least a few months
after exposure, but the subjects generally have been exposed to heavy levels of lead that could
affect bone metabolism (Lindh et al., 1978; Flood et al., 1988). Burial of lead beneath thesurfaces in regions of bone formation has been observed, and there is evidence that lead is
eventually distributed throughout the bone volume (Vincent, 1957; Lacroix, 1960; ScheimanTagger and Brodie, 1964; Hong et al., 1968; Yen and Shaw, 1977; Lindh et al., 1978; Hu etal., 1989). In beagles, long-term skeletal retention of lead is similar to that of strontium andradium (Hursh, 1973; Lloyd et al, 1975). Because lead is incorporated into the bone crystal,
long-term losses from bone presumably are largely controlled by the rate of bone resorption.
(456) In a study of the comparative behaviour of injected lead, calcium, and barium inbone of rabbits, Domanski and Trojanowska (1980) found that the build-up of lead in bone is151

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5992
5993
5994
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5996

5997
5998
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6001
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6003
6004

similar to that of barium and greater than that of calcium when related to integrated activity inplasma. Similar results for lead and calcium were obtained by Heard and Chamberlain (1984)
for humans injected with radioisotopes of these two elements. A relatively low uptake of leadby the skeleton at early times compared with radium, for example, apparently reflects acompetition for lead with RBC that does not occur to a significant extent for the alkaline earth
elements. The later build-up in the skeleton results from the gradual release of activity from
RBC and the relatively longer retention of lead in the skeleton than in RBC.
9.2.3.2. Biokinetic model for systemic lead
(457) The biokinetic model for systemic lead used in this report is the model applied toadult members of the public in ICRP Publication 67 (1993) and to workers in Publication 68(1994). The model is a simplification of a model of Leggett (1993), which provides moredetail concerning the initial exchange of lead between plasma and extravascular spaces, its
kinetics in RBC, and its distribution in soft tissues.
(458) The model structure is shown in Figure 9-1. Parameter values for a reference worker
are listed in Table 9-2. Lead-specific parameter values (all parameter values other than those
based on bone remodeling rates) were based on results of: controlled studies of on humansubjects receiving stable or radioactive lead by injection, acute inhalation, or acute ingestion;
long-term balance studies on human subjects; autopsy measurements on environmentally
exposed humans; bioassay and autopsy measurements on occupationally exposed persons;and radioisotopic studies on laboratory animals, primarily non-human primates and dogs.

Figure 9-1. Structure of the biokinetic model for systemic lead. Abbreviations: RBC = Red Blood
Cells, Exch = Exchangeable, Nonexch = Non-exchangeable.
The primary parameter values such as compartment deposition fractions and biological half-times underlying thetransfer coefficients given in Table 9-3 are summarized below. The reader is referred to the paper by Leggett(1993) for a detailed discussion of the conceptual basis of the model and the data sets used in the development ofparameter values.

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(459) An early, rapid exchange of lead that occurs between plasma and extravascularspaces (Leggett, 1993) is not addressed in the present model. It is assumed here that lead
leaves plasma at a rate of 70 d-1 and that a substantial portion of activity leaving plasma goesto a rapid-turnover soft tissue compartment called ST0 that is three times as large as theplasma compartment. Inflow and outflow rates selected for RBC yield an estimate of roughly
58% of injected lead in RBC at l-2 days after injection. It is assumed that 40% of outflow
from plasma deposits in RBC. A biological half-time of 5 d for lead in RBC is set to yield a
net half-time in blood (elongated by recycling) of about 20 days in the time between a few
days and a few weeks after injection, based on data for humans.

Table 9-3. Transfer coefficients in the biokinetic model for systemic lead
From
PlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaRBC
Trabecular bone surface
Trabecular bone surface
Cortical bone surface
Cortical bone surface
Exch trabecular bone volume
Exch trabecular bone volume
Exch cortical bone volume
Exch cortical bone volume
Nonexch trabecular bone volume
Nonexch cortical bone volume
Liver 1
Liver 1
Liver 1
Liver 2Urinary path
Other kidney tissue
ST0
ST1
ST2
ST1

To
Urinary bladder content
Right colon content
Trabecular bone surface
Cortical bone surface
ST0
ST1
ST2
Liver 1
Urinary path
Other kidney tissue
RBC
Excreta (sweat)
PlasmaPlasmaExch trabecular bone volume
PlasmaExch cortical bone volume
Trabecular bone surface
Nonexch trabecular bone volume
Cortical bone surface
Nonexch cortical bone volume
PlasmaPlasmaPlasmaSI content
Liver 2
PlasmaUrinary bladder content
PlasmaPlasmaPlasmaPlasmaExcreta (Hair, skin, nails)

Transfer oefficient
(d-1)
1.75
0.7
4.86
3.89
22.16
0.7
0.14
4.9
2.45
0.0245
28
0.42
0.139
0.5
0.5
0.5
0.5
0.01850.00460.01850.00460.000493
0.0000821
0.03120.03120.006930.00190.139
0.00197.39
0.004160.00038
0.00277

RBC = Red Blood Cells, Exch = Exchangeable, Nonexch = Non-exchangeable
6015
6016

(460) Urinary and faecal excretion rates were based on observations of the fate of153

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intravenously injected radiolead in human subjects. It is assumed that 6% of outflow fromplasma enters urinary excretion pathways. Part of this (2.5%) is assumed to passinstantaneously through the kidneys to the bladder content, and the rest (3.5%) is assumed todeposit in the renal tubules and to be released to the bladder content over a period of days. It
is assumed that 1.7% of outflow from plasma enters the intestinal content either directly or
indirectly: 1% passes directly into the right colon content, and 10% of the deposition in liver(7% of outflow from plasma) is secreted into the SI content. Because lead entering the SI
content is subject to reabsorption to blood, the model predicts that slightly less than 1.7% ofoutflow from plasma is excreted in faeces.
(461) Loss of lead in sweat is assumed to represent 0.6% of outflow from plasma. A
fourth excretion pathway, representing loss of lead in hair, skin, and nails, is depicted as
outflow from soft-tissue compartment ST1 (described below). The predicted loss of leadfrom the body through this fourth pathway is equivalent to 0.4% of outflow from plasma.
(462) The liver is assumed to consist of two compartments, one with relatively shortretention (Liver 1) and one with relatively long retention (Liver 2). Activity entering the liveris assigned to Liver 1. A small portion of the activity leaving Liver 1 is assigned to Liver 2,
but most of the outflow is divided between plasma and the small intestine. Parameter values
describing uptake, retention, and removal of lead by the liver were based on biokinetic studiesof radiolead in human subjects, baboons, and dogs, and blood-to-liver concentration ratios
observed in persons chronically exposed to low levels of environmental lead. It is assumed
that 7% of lead leaving plasma deposits in Liver 1; the removal half-time from Liver 1 is 10
days; 10% of activity leaving Liver 1 deposits in Liver 2; and the remaining 90% of outflow
from Liver 1 is evenly divided between plasma and SI content. The removal half-time from
Liver 2 is 1 y.
(463) The kidneys are assumed to consist of two compartments, one with relatively shortretention (Urinary path) and one with relatively long retention (Other kidney tissue). The
Urinary path receives lead from plasma and loses activity to the urinary bladder content.
Other kidney tissue exchanges lead slowly with plasma. Parameter values describing uptake,retention, and removal of lead by the kidneys were based on biokinetic studies of radiolead inbaboons, dogs, and rats, and blood-to-liver concentration ratios observed in persons
chronically exposed to low levels of environmental lead. It is assumed that 3.5% of outflow
from plasma deposits in the urinary path and 0.035% deposits in other kidney tissue. The
removal half-time from the urinary path to the urinary bladder content is 5 d. The removal
half-time from other kidney tissue is 1 y.
(464) Other soft tissues are divided into compartments ST0, ST1, and ST2 representing
fast (hours), moderate (months), and slow (years) return of lead to plasma. These are notphysically identifiable compartments. They are defined on a kinetic basis, for reasonableagreement with estimates of the lead content of soft tissues other than liver and kidneys
during chronic exposure or as a function of time after acute intake of lead. The underlying
datasets include results of a variety of studies on laboratory animals and human subjects.
Compartments ST1 and ST2 are assigned 1% and 0.2% of outflow from plasma, respectively.
The fast-turnover compartment is assigned 31.66% of outflow from plasma, where the last
three digits reflect an adjustment of the initially assigned deposition fraction to account for
100% of outflow from plasma. The biological half-times in ST0, ST1, and ST2 areapproximately 2.25 h, 100 d, and 5 y, respectively. Outflow from the intermediate-term
compartment ST1 is divided between plasma (60%) and an excretion compartment
representing loss of lead in hair, skin, and nails (40%).
(465) Parameter values describing the bone kinetics of lead at early to intermediate times
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after uptake to blood are based on studies of radiolead in adult humans, baboons, and dogs,
and analogy with radium. Bone surface is assumed to receive 12.5% of outflow from plasma.
The assumed division between trabecular and cortical surface is based on analogy withradium. Lead is removed from bone surface at a rate of 1 d-1, with 50% returning to plasma
and 50% entering exchangeable bone volume. The rates of transfer from the exchangeablebone volume compartments to bone surface and to non-exchangeable bone volume are basedon analogy with radium. The assumed rate of removal from each bone volume compartment
to plasma is the reference bone turnover rate for that bone type (ICRP, 2002a).
9.2.3.3. Treatment of radioactive progeny
Dosimetrically significant lead progeny(466) Several lead isotopes addressed in this report have radioactive progeny that
contribute significantly to dose coefficients for the internally deposited lead parent. The
dosimetrically significant members of lead chains are isotopes of gold, mercury, thallium,
lead, bismuth, or polonium. The biokinetic models applied to these elements as progeny ofsystemic lead are described below.
Gold(467) The biokinetics of gold has been investigated extensively in human subjects andlaboratory animals in studies related to its medical applications, particularly the use of stablegold for treating rheumatoid arthritis and short-lived radioactive gold as an imaging agent(Freyberg, et al., 1942; Block, et al., 1942, 1944; Jeffrey et al., 1958; Lawrence, 1961; Rubinet al., 1967; McQueen and Dykes, 1969; Mascarenhas et al., 1972; Sugawa-Katayama et al.,
1975; Gottlieb, 1979, 1983; Jellum et al., 1980; Massarella and Pearlman, 1987; Andersson etal., 1988; Bacso et al., 1988; Brihaye and Guillaume, 1990). Also, several studies haveaddressed the biological behavior of gold as a radioactive contaminant in the workplace orenvironment (Durbin, 1960; Fleshman et al., 1966; Chertok and Lake, 1971a, 1971b, 1971c;
Silva et al., 1973). Development of a representative biokinetic model for systemic gold in
adult humans is complicated by the apparent dependence of reported data on the mode ofadministration, chemical form, administered mass, and other study conditions. The following
general properties appear to be typical of gold administered in relatively soluble form. Muchof the gold reaching blood is excreted in the first week or two, but a nontrivial portion isretained for several weeks or months. Excretion is primarily in urine. Most of the retained
amount is found in the kidneys, liver, and blood. Most of the gold found in blood is bound toplasma proteins.
(468) The following model is applied in this report to radioisotopes of gold produced insystemic compartments following intake of a lead parent. Gold leaves the central bloodcompartment (Blood 1) at the rate 1 d-1 and is distributed as follows: 10% to Blood 2 (a bloodcompartment with relatively slow turnover), 30% to Urinary bladder content, 10% to Rightcolon content, 10% to Kidneys, 10% to Liver, 5% to Red marrow (active marrow), 1% toSpleen, 1% to Trabecular bone surface, 1% to Cortical bone surface, 0.06% to Testes, 0.02%
to Ovaries, 10% to ST2 (a soft tissue compartment with slow turnover), and the remaining
11.92 % to ST1 (a soft tissue compartment with a moderate turnover time). Gold transfersfrom Blood 2 to Blood 1 with a half-time of 5 d; from Liver, ST1, Spleen, Testes, Ovaries,
Red marrow, Trabecular bone surface, and Cortical bone surface to Blood 1 with a half-timeof 10 d; from Kidneys to Urinary bladder content with a half-time of 10 d; and from Other 2
to Blood with a half-time of 50 d. Gold produced by radioactive decay in a blood
155

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compartment that is not identifiable with a blood compartment of the gold model is assumed
to transfer to Blood 1 at the rate 1000 d-1. Gold produced in a soft-tissue compartment that is
not identifiable with a compartment in the gold model is assumed to transfer to Blood 1 witha half-time of 10 d. Gold produced in a compartment of trabecular or cortical bone volume isassumed to transfer to Blood 1 at the reference turnover rate for that bone type.
Mercury(469) The model for mercury produced in systemic compartments by radioactive decay isbased on biokinetic data for human subjects and laboratory animals exposed to inorganic
forms of mercury, primarily divalent mercury salts (Friberg, 1956; Rothstein and Hayes,
1960; Cember, 1962; Hayes and Rothstein, 1962; Berlin and Ullberg, 1963; Clarkson andRothstein, 1964; Joselow et al., 1967; Johnson and Johnson, 1968; Berlin et al., 1969; Brown
et al., 1975; Jugo, 1976; Hursh et al., 1976, 1980; Cherian et al., 1978; Berlin, 1986; Newton
and Fry, 1978; Jonsson et al., 1999). Retention data for mercury entering the body as a vapor
are also considered for times remote from intake, as the biokinetics of this initial form of
mercury gradually converges to that seen after intake of divalent mercury salts. Studies ofanimals administered divalent mercury salts indicate initially rapid disappearance of mercury
from blood, but a substantial portion of the injected amount is retained in blood after several
hours. Animal and human studies indicate that as much as 30-40% of divalent mercury
reaching blood is deposited in the kidneys and is retained there with a half-time on the orderof 50 (35-90) d. In rats injected with inorganic divalent mercury, the kidneys and liveraccounted for about 10% of the systemic burden after 4 h, 40% after 1 d, 70% after 6 d, 88%
after 15 d, and 91% after 52 d. In human subjects, more than half of absorbed inorganic
mercury is removed from the body in urine. Initially, the rate of fecal excretion is muchhigher than that of urinary excretion, but this relation reverses over a few weeks as the kidneycontent builds up and the content of other systemic tissues declines. In addition to losses inurine and faeces, mercury is removed from the systemic fluids and tissues by exhalation as
mercury vapor, and small amounts are lost through sweat, hair, and other routes. Externalmeasurements on human subjects exposed to inorganic mercury suggest that much of themercury deposited in soft tissues other than kidneys is removed over a period of a few weeks.
In rats receiving mercury chloride by intravenous or intramuscular injection, a slow phase of
excretion with a half-time of 3 mo or more was apparent by 2 mo after injection. A
component of retention in the body with a half-time on the order of 100 d is also indicated bylong-term measurements of urinary mercury following human exposure to inorganic mercury.
(470) The systemic model for mercury as a member of a lead chain consists of thefollowing compartments: Plasma 1 (diffusible mercury), Plasma 2 (protein-bound mercury),
RBC, Kidneys, Liver, Spleen, Red marrow (active marrow), Testes, Ovaries, Cortical bone
surface, Trabecular bone surface, and compartments ST1 and ST2 representing two phases ofloss from remaining soft tissues. Mercury absorbed to blood or reentering blood from tissues
is assigned to Plasma 1. The total transfer coefficient from Plasma 1 to all destinations is16.636 h-1 corresponding to a half-time of 1 h. Outflow from Plasma 1 is divided as follows:
4% to RBC, 12% to Plasma 2, 35% to Kidneys, 20% to Liver, 10% to Small intestine content,
3% to Red marrow, 0.6% to Spleen, 0.036% to Testes, 0.012% to Ovaries, 3.5% to ST2, 5%
to Excreta (excretion other than urine and faeces), 1% to Cortical bone surface, 1% toTrabecular bone surface, and the remaining 4.852% to ST1. Mercury transfers from RBC to
Plasma 1 with a half-time of 3 d, from Plasma 2 to Plasma 1 with a half-time of 1 d, from
Kidneys to Urinary bladder content with a half-time of 35 d, from bone surface compartments
to Plasma 1 with a half-time of 20 d, from ST1 to Plasma 1 with a half-time of 20 d, and from156

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ST2 to Plasma 1 with a half-time of 100 d. Mercury is removed from Liver with a half-timeof 10 d, with outflow from Liver equally divided between Plasma 1 and SI content. Mercury
transfers from Red marrow, Spleen, Testes, and Ovaries to Plasma 1 with a half-time of 20 d.
Mercury is absorbed from SI content to Plasma 1 based on the reference absorption fraction
for ingested inorganic mercury, and the unabsorbed portion transfers to the Right colon
content and is eventually excreted in faeces. Mercury produced in a soft-tissue compartmentthat is not identifiable with a compartment in the mercury model is assumed to transfer to thecentral blood compartment of the mercury model with a half-time of 20 d. Mercury produced
in a compartment of cortical or trabecular bone volume is assumed to transfer to the central
blood compartment at the reference turnover rate for that bone type.
Thallium(471) The biokinetics of thallium has been investigated extensively in human subjects andlaboratory animals, due mainly to the importance of radio-thallium in nuclear medicine andmany occurrences of accidental or malicious poisoning with stable thallium (Gettler andWeiss, 1943; Barclay et al., 1953; Lie et al., 1960; Gehring and Hammond, 1967; Potter et al.,
1971; Bradley-Moore et al., 1975; Strauss et al., 1975; Atkins et al., 1977; Suzuki et al., 1978;
Berger et al., 1983; Nakamura et al., 1985; Gregus and Klaassen, 1986; Krahwinkel et al.,
1988; Lathrop et al., 1989; Blanchardon et al., 2005). Comparisons of the disappearance ofradioisotopes of thallium, potassium, and rubidium from blood and their uptake by tissues oflaboratory animals suggest a close relation in the movement of these elements, presumably
associated with their similar ionic radii (Gehring and Hammond, 1967; Strauss et al., 1975).
These elements are rapidly removed from plasma, and their early distributions are determinedlargely by the distribution of cardiac output. After entering the cell, thallium is released more
slowly than potassium or rubidium, but the mean residence time of thallium in the body isless than that of potassium or rubidium due to a higher rate of clearance from plasma to
excretion pathways. Most reported removal half-times of thallium from the adult human bodyare in the range 9-13 d (Atkins et al., 1977; Krahwinkel et al., 1988; Blanchardon et al.,2005). Chen et al. (1983) reported two components of retention of thallium: 7d for 63% and
28 d for 37% of the injected amount. It appears that faecal excretion typically represents
more than half of cumulative excretion of thallium over a period of weeks following its acuteintake, although some relatively short-term human studies have suggested that excretion ofthallium is primarily in urine (cf. Barclay et al., 1953; Lathrop et al., 1975; Atkins et al.,
1977; Blanchardon et al., 2005).
(472) The following model is applied in this report to radioisotopes of thallium produced
in systemic compartments following intake of a lead parent. Thallium leaves the central
blood compartment (Plasma) at the rate 200 d-1 (corresponding to a half-time of 5 min) and is
distributed as follows: 2.5% to RBC, 0.75% to Urinary bladder content, 1.75% to Right colon
content, 5% to Kidneys, 5% to Liver, 1.5% to Red marrow (active marrow), 0.2% to Spleen,
0.045% to Testes, 0.015% to Ovaries, 7.5% to Trabecular bone surface, 7.5% to Cortical bone
surface, and 68.24% to ST0 (remaining soft tissues). Thallium returns from RBC to Plasma
at the rate 3.7 d-1 and from tissue compartments to Plasma at the rate 2.5 d-1. Thallium
produced by radioactive decay in a blood compartment that is not identifiable with a bloodcompartment of the thallium model is assumed to transfer to Plasma at the rate 1000 d-1.
Thallium produced in a soft-tissue compartment that is not identifiable with a compartment of
the thallium model is assumed to transfer to Plasma at the rate 2.5 d-1. Thallium produced in
a compartment of cortical or trabecular bone volume is assumed to transfer to Plasma at thereference turnover rate of that bone type.
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Lead
(473) The systemic model for lead as a progeny of a lead parent is based on thecharacteristic model for lead applied in this series of reports. The structure of thecharacteristic model is modified by the addition of four compartments that are explicitly
identified in models for some elements appearing in lead chains: Red marrow (active
marrow), Spleen, Testes, and Ovaries. Each of these compartments is assumed to exchange
lead with the central blood compartment of the lead model (Plasma). Transfer coefficients forthe added compartments are selected for reasonable consistency with the biokinetic database
underlying the characteristic model for lead and with the retention curve for total soft tissues
based on the characteristic model. The specific changes to the characteristic model for leadare as follows: (1) the transfer coefficients from Plasma to compartments added to thecharacteristic model for lead are 0.015 d-1 for Red marrow, 0.002 d-1 for Spleen, 0.00045 d-1
for Testes, and 0.00015 d-1 for Ovaries; (2) the transfer coefficient from Plasma to ST1 isreduced from 0.70 d-1 to 0.69 d-1, and the coefficient from Plasma to ST2 is reduced from
0.14 d-1 to 0.138 d-1; and (3) the assigned transfer coefficient from each of the added
compartments back to Plasma is 0.002 d-1. Lead produced in a blood compartment of apreceding chain member that is not identifiable with a blood compartment of the lead modelis assigned the transfer rate 1000 d-1 to Plasma.
Bismuth(474) The systemic model for bismuth as a progeny of lead is based on the characteristic
model for bismuth applied in this series of reports. The structure of the characteristic model
is modified by the addition of four compartments that are explicitly identified in models forsome elements appearing in lead chains: Red marrow (active marrow), Spleen, Testes, andOvaries. Each of these compartments is assumed to exchange bismuth with the central bloodcompartment (plasma). Transfer coefficients are selected for reasonable consistency with the
biokinetic database underlying the characteristic model for bismuth and with the retention
curve for total soft tissues based on that original model. The specific changes to thecharacteristic model for bismuth are as follows: (1) the transfer coefficients from plasma to
the added compartments are 0.3 d-1 for Red marrow, 0.02 d-1 for Spleen, 0.003 d-1 for Testes,and 0.001 d-1 for Ovaries; (2) the transfer coefficient from plasma to the Other soft-tissuecompartment ST1 is reduced from 4.2 d-1 to 3.976 d-1, and the coefficient from plasma to the
Other soft tissue compartment ST2 is reduced from 1.3 d-1 to 1.2 d-1; and (3) the assigned
transfer coefficient from each of the added compartments back to plasma is 0.007 d-1 (halftime of 100 d). Bismuth produced in a blood compartment that is not identifiable with acompartment of the bismuth model is assumed to transfer to the plasma compartment of thebismuth model at the rate 1000 d-1. Bismuth produced in a trabecular or cortical bone volume
compartment is assumed to transfer to plasma at the reference turnover rate for that bone type.
Polonium(475) The model for polonium produced in systemic compartments following intake of alead isotope is a simplified version of the model applied in this report to polonium absorbed
to blood following its inhalation as a parent radionuclide. It is assumed that polonium leaves
the central blood compartment of the model (Plasma) at the rate 100 d-1 and distributes asfollows: 5% to red blood cells (RBC), 3% to plasma proteins (Plasma P), 28% to Liver, 28%
to Kidneys, 1.2% to Bone surface, 3.3% to Red marrow (active marrow), 1.6% to Spleen,
0.1% to Testes, 0.05% to Ovaries, 4% to a soft-tissue compartment with a relatively long158

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retention time (ST2), and the remaining 25.755% to a soft-tissue compartment with arelatively short retention time (ST1). Activity entering Liver is equally divided between
compartments Liver 1 and Liver 2. Of the 28% of outflow from Plasma depositing in
Kidneys, 24% is assigned to the urinary path (Kidneys 1) and 4% is assigned to other kidney
tissue (Kidneys 2). Activity entering Bone surface is equally divided between Cortical bone
surface and Trabecular bone surface. Activity transfers to Plasma from each of thecompartments RBC, Plasma P, ST1, Liver 2, Red marrow, Spleen, and Kidneys 2 with a halftime of 7 d. Activity transfers from Liver 1 to Small intestine content with a half-time of 5 d,from Kidneys 1 to Urinary bladder content with a half-time of 4 d, from Trabecular andCortical bone surface to Plasma with a half-time of 30 d, from ST2 to Plasma with a half-timeof 100 d, and from Testes and Ovaries to Plasma with a half-time of 50 d. Polonium
produced in a soft-tissue compartment of a preceding chain member that is not identifiablewith a compartment in the polonium model is assumed to move to Plasma with a half-time of
7 d. Polonium produced in a compartment of cortical or trabecular bone volume is assumed totransfer to Plasma at the reference rate of turnover of that bone type.
9.3.

Individual monitoring

210

Pb(476) Urine bioassay is used for the monitoring of 210 Pb. In addition, when necessary,measurements of the concentration in faeces may be performed. For refined monitoring of 210
Pb skeleton burdens, in vivo measurements of the cranium and knee might be performed.
IsotopeMonitoring
Technique

MethodMeasurement

210

Pb

Urine Bioassay

210

Pb

Faeces Bioassay

210

Pb

210

Pb

Cranium
Measurement
Knee
Measurementof Typical
Detection
Limit
Beta proportional 0.1 Bq/L
counting
Beta proportional 0.04 Bq/24h
counting
γ-ray spectrometry

Achievabledetection limit

γ-ray spectrometry

14 Bq

0.01 Bq/L

16 Bq

212

Pb
(477) In vivo monitoring, lung and Whole Body Counting, are the main techniques used todetermine 212 Pb intakes.
IsotopeMonitoring
Technique

212

Pb

212

Pb

Whole
Counting
Lung Counting

MethodMeasurementof Typical
Detection
Limit
Body γ-ray spectrometry 80 Bq
γ-ray spectrometry

214

9 Bq

Achievabledetection limit
50Bq
8Bq

Pb
(478) In vivo monitoring, lung and Whole Body Counting, are the main techniques used todetermine 214 Pb intakes
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IsotopeMonitoring
Technique

214

Whole
Counting
Lung Counting

Pb

214

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6322
6323
6324
6325
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6330
6331
6332
6333

Pb

MethodMeasurementof Typical
Detection
Limit
Body γ-ray spectrometry 90 Bq
γ-ray spectrometry

Achievabledetection limit
50 Bq

16 Bq

References
Andersson, L.; Hallstadius, L.; Strand, S.-E. 1988. Biokinetics and dosimetry for 195Au, evaluated in
an animal model. Eur. J. Nucl. Med. 14:393-399.
Atkins, H. L.; Budinger, T. F.; Lebowitz, E.; Ansari, A. N.; Greene, M. W.; Fairchild, R. G.; Ellis, K.
J. 1977. Thallium-201 for medical use, 3. Human distribution and physical imaging
properties. J. Nucl. Med. 18:133-140.
Bacso, J.; Uzonyi, I.; Dezso, B. 1988. Determination of gold accumulation in human tissues causedby gold therapy using x-ray fluorescence analysis. Appl. Radiat. Isot. 39:323-326.
Ballou, J.E., Gies, R.A., Case, A.C., Haggard, D.L., Buschbom, R.L., Ryan, J.L., 1986. Depositionand early disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat. HealthPhys. 51, 755–771.
Ballou, J.E., Hursh, J.B., 1972. The measurement of thoron in the breath of dogs administeredinhaled or injected ThO2. Health Phys., 22, 155–159.
Barclay, R. K.; Peacock, W. C.; Karnofsky, D. A. 1953. Distribution and excretion of radioactive
thallium in the chick embryo, rat, and man. J. Pharmacol. Exp. Ther.107:178-187.
Barry, P.S.I., 1975. A comparison of lead concentrations in human tissues. Br. J. Znd. Med. 32, 119139.
Barry, P.S.I., 1981. Concentrations of lead in tissues of children. Br. J. Ind. Med. 38, 61-71.
Berger, C. D.; Lane, B. H.; Hamrick, T. 1983. Clearance of 202Tl contaminate following intravenous
injection of 201Tl. Health Phys. 45:999-1001.
Berlin, M. (1986) Mercury. In: Friberg, L.; Nordberg, G. F.; Vouk, V. B., eds. Handbook of the
toxicology of metals, Vol. II. New York: Elsevier; 387-445.
Berlin, M.; Fazackerley, J.; Nordberg, G. 1969. The uptake of mercury in the brains of mammals
exposed to mercury vapor and to mercuric salts. Arch. Environ. Health 18, 719-729.
Berlin, M.; Ullberg, S. (1963) Accumulation and retention of mercury in the mouse. Arch. Environ.
Health 6, 589-601.
Bianco, A., Gibb, F.R., Morrow, P.E., 1974. Inhalation study of a submicron size lead-212 aerosol.
In: Snyder, W.S. (Ed.), 3rd Int. Congress of the IRPA, Washington D.C., 9–14 Sept. 1973.,
USAEC CONF-730907, pp. 1214–1219.
Blake, K., 1976. Absorption of lead-203 From gastrointestinal tract of man. Enviromental Research.
11, 1-4.
Blanchard, R.L., Moore, J.B., 1971. Body burden, distribution and internal dose of Pb-210 and Po210 in a uranium miner population. Health Phys. 21, 499-518.
Blanchard, R. L., Moore, J.B., 1970. Pb-210 and Po-210 in tissues of some Alaskan residents as
related to consumption of caribou or reindeer meat. Health Phys. 18, 127-134.
Block, W. D.; Buchanan, O. H.; Freyberg, R. H. (1942). Metabolism, toxicity and manner of action ofgold compounds used in the treatment of arthritis. IV. Studies of the absorption, distribution
and excretion of gold following the intramuscular injection of gold thioglucose and gold
calcium thiomalate. J. Pharmacol. Exp. Ther. 76:355-357.
Block, W. D.; Buchanan, O. H.; Freyberg, R. H. (1944). Metabolism, toxicity and manner of action ofgold compounds used in the treatment of arthritis. V. A comparative study of the rate of160

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6363
6364
6365
6366
6367
6368
6369
6370
6371
6372
6373
6374
6375
6376
6377
6378
6379
6380
6381
6382
6383
6384

absorption, the retention, and the rate of excretion of gold administered in different
compounds. J. Pharmacol. Exp. Ther. 82, 391-398.
Booker, D.V., Chamberlain, A.C., Newton, D., Stott, A.N., 1969. Uptake of radioactive leadfollowing inhalation and injection. Br. J. Radiol. 42, 457–466.
Boudene, C., Malet, D., Masse, R., 1977. Fate of 210Pb inhaled by rats. Toxicol. Appl. Pharmacol.
41, 271–276.
Bradley-Moore, P. R.; Lebowitz, E.; Greene, M. W.; Atkins, H. L.; Ansari, A. N. (1975). Thallium201 for medical use, 2. Biologic behavior. J. Nucl. Med. 16:156-160.
Brihaye, C.; Guillaume, M. (1990). 195Au biokinetics and dosimetry. Eur. J. Nucl. Med. 16:369-371.
Brown, K. W.; McFarlane, J. C.; Bernhardt, D. E. (1975) Accidental inhalation of mercury-203.
Health Phys. 28, 1-4.
Butterweck, G., Schuler, C., Vezzu, G., Muller, R., Marsh, J.W., Thrift, S., Birchall, A., 2002.
Experimental determination of the absorption rate of unattached radon progeny from
respiratory tract to blood. Radiat. Prot. Dosimetry, 102, 343–348.
Butterweck, G., Vezzù, G., Schuler, Ch., Müller, R., Marsh, J.W., Thrift, S., Birchall, A., 2001. Invivo measurement of unattached radon progeny deposited in the human respiratory tract.
Radiat. Prot. Dosim. 94, 247–250.
Cember, H. (1962) The influence of the size of the dose on the distribution and elimination of
inorganic mercury, Hg(NO3)2, in the rat. Amer. Ind. Hyg. Assoc. J. 23, 304-313.
Chamberlain, A.C., Clough, W.S., Heard, M.J., Newton, D., Stott, A.N.B., Wells, A.C., 1975. Uptakeof lead by inhalation of motor exhaust. Proc. R. Soc. Lond. B. 192, 77–110.
Chamberlain, A.C., Heard, M.J., Little, P., Newton, D., Wells, A.C., Wiffen, R.D., 1978.
Investigations into lead from motor vehicles. UK Atomic Energy Authority Report AERE-R
9198. HMSO, London.
Chen, C. T.; Lathrop, K. A.; Harper, P. V.; Bartlett, R. D.; Stark V. J.; Fultz, K. R.; Faulhaber, P. F.
(1983). Quantitative measurement of long term in vivo thallium distribution in the human. J.
Nucl. Med., 24:P50.
Cherian, M. G.; Hursh, J. B.; Clarkson, T. W.; Allen, J. (1978) Radioactive mercury distribution in
biological fluids and excretion in human subjects after inhalation of mercury vapor. Arch.
Environ. Health 33, 109-114.
Chertok, R. J.; Lake, S. (1971a) Availability in the peccary pig of radionuclides in nuclear debris
from the plowshare excavation buggy. Health Phys. 20, 313-316.
Chertok, R. J.; Lake, S. (1971b) Biological availability of radionuclides produced by the plowshare
event schooner - I. Body distribution in domestic pigs exposed in the field. Health Phys. 20,
317-324.
Chertok, R. J.; Lake, S. (1971c) Biological availability of radionuclides produced by the plowshare
event schooner - II. Retention and excretion rates in peccaries after a single oral dose ofdebris. Health Phys. 20, 325-330.
Clarkson, T.; Rothstein, A. (1964) The excretion of volatile mercury by rats injected with mercuric
salts. Health Phys. 10, 1115-1121.
Cohen, B.S., Eisenbud, M., Wrenn, M.E., Harley, N.H., 1979. Distribution of polonium-210 in thehuman lung. Radiat. Res. 79, 162-168.
Cohen, B.S., Harley, N.H., Tso, T.C., 1985. Clearance of polonium-210-enriched cigarette smokefrom the rat trachea and lung. Toxicol. Appl. Pharmacol. 79, 314-322.
Cohen, N., Eisenbud, M., Wrenn, M.E., 1970. The Retention and Distribution of Lead-210 in the
Adult Baboon. Progress report, Radioactivity studies, New York University Medical Center,
New York.
Desideri D., Meli, M.A., Feduzi, L., Roselli, C., 2007. 210Po and 210Pb inhalation by cigarettesmoking in Italy. Health Phys. 92(1) 58-63.
DeSilva, P.E., 1981. Determination of lead in plasma and studies on its relationship to lead inerythrocytes. Br. J. Ind. Med. 38,209-217.

161

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6385
6386
6387
6388
6389
6390
6391
6392
6393
6394
6395
6396
6397
6398
6399
6400
6401
6402
6403
6404
6405
6406
6407
6408
6409
6410
6411
6412
6413
6414
6415
6416
6417
6418
6419
6420
6421
6422
6423
6424
6425
6426
6427
6428
6429
6430
6431
6432
6433
6434
6435

Domanski, T., Trojanowska, B., 1980. Studies on metabolic kinetics of lead and alkaline earth
elements (Ca, Ba). Acta Physiol. Pol. 31, 439-447.
Drew, R.T., 1971. 212Pb distribution studies in the rat. Health. Phys. 20, 617–623.
Duport, P., Robertson, R., Ho, K., Horvat, F., 1991. Flow-through dissolution of uranium-thorium ore
dust, uranium concentrate, uranium dioxide, and thorium alloy in simulated lung fluid.
Radiat. Prot. Dosim. 38(1/3), 121-133.
Durbin, P. W. (1960) Metabolic characteristics within a chemical family. Health Phys. 2, 225-238.
Everson, J., Patterson, C.C., 1980. "Ultra-clean" isotope dilution/mass spectrometric analyses for leadin human blood plasma indicate that most reported values are artificially high. Clin. Chem.
26, 1603-1607.
Fleshman, D; Krotz, S.; Silva, A. (1966). The metabolism of elements of high atomic number. UCRL
14739:69-86.
Flood, P.R., Schmidt, P.F., Wesenberg, G.R., Gadeholt, H., 1988. The distribution of lead in human
hemopoietic tissue and spongy bone after lead poisoning and Ca-EDTA chelation therapy.
Arch. Toxicol. 62, 295-300.
Freyberg, R. H.; walter d. Block, W. D.; Levey, S. (1942). Metabolism, toxicity and manner of actionof gold compounds used in the treatment of arthritis. III. Complete excretion studies andcomparison of intravenous and intramuscular administration of some gold salts. Ann.
Rheum. Dis. 3:77-89.
Friberg, L. (1956) Studies of the accumulation, metabolism and excretion of inorganic mercury(203Hg) after prolonged subcutaneous administration to rats. Acta Pharmacol. et Toxicol.
12, 411-427.
Gehring, P. J.; Hammond, P. B. (1967). The interrelationship between thallium and potassium inanimals. J. Pharmacol. Exp. Ther. 155:187-201.
Gettler, A. O.; Weiss, L. (1943). Thallium poisoning. III. Clinical toxicology of thallium. Amer. J.
Clin. Pathol. 13: 422-429.
Gottlieb, N. L. (1983). Comparison of the kinetics of parenteral and oral gold. Scand. J. Rheumatol.
12:10-14.
Greenhalgh, J.R., Birchall, A., James, A.C., Smith, H., Hodgson, A., 1982. Differential retention of
212Pb ions and insoluble particles in nasal mucosa of the rat. Phys. Med. Biol. 27, 837–
851.
Greenhalgh, J.R., James, A.C., Smith, H., Hodgson, A., 1979. Absorption of lead ions from the lung.
NRPB/ R&D3. Annual Research and Development Report 1978 pp. 38–42.
Greenhalgh, J.R., James, A.C., Smith, H., Stubberfield, D.R., 1978. Absorption of lead from thebronchial region of the lung. NRPB/ R&D2. Annual Research and Development Report
1977 pp. 65–70.
Gregus, Z.; Klaassen, C. D. 1986. Disposition of metals in rats: A comparative study of fecal, urinary,and biliary excretion and tissue distribution of eighteen metals. Toxicol. Appl. Pharmacol.
85:24-38.
Griffin, R.M., Matson, W.R., 1972. The assessment of individual variability to trace metal insult:low-molecular-weight metal complexing agents as indicators of trace metal insult. Amer.
Indus. Hyg. Assoc. 33, 373-377.
Gross, S.B., Pfitzer, E.A., Yeager, D.W., Kehoe, R.A., 1975. Lead in human tissues. Toxicol. Appl.
Pharmacol. 32, 638-651.
Habibi, K., 1973. Characterisation of particulate matter in vehicle exhaust. Environ. Sci. Technol. 7,
223–234.
Hamilton, E.I., Minski, M.J., Cleary, J.J., 1972. The concentration and distribution of some stableelements in healthy human tissues from the United Kingdom. Sci. Total Environ. 1, 341374.
Hayes, A. D.; Rothstein, A. 1962. The metabolism of inhaled mercury vapor in the rat studied byisotope techniques. J. Pharmacol. 38, 1-10.

162

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6436
6437
6438
6439
6440
6441
6442
6443
6444
6445
6446
6447
6448
6449
6450
6451
6452
6453
6454
6455
6456
6457
6458
6459
6460
6461
6462
6463
6464
6465
6466
6467
6468
6469
6470
6471
6472
6473
6474
6475
6476
6477
6478
6479
6480
6481
6482
6483
6484
6485
6486

Heard, M., Chamberlain, A., 1982. Effect of minerals and food on uptake from the gastrointestinal
tract in humans. Human Toxicology. 1. 411–415.
Heard, M.J., Chamberlain, A.C., 1984. Uptake of Pb by human skeleton and comparative metabolismof Pb and alkaline earth elements. Health Phys. 47,857-865.
Heard, M.J., Wells, A.C. Newton, D., Chamberlain, A.C., 1979. Human uptake and metabolism of
tetra-ethyl and tetra-methyl lead vapour labelled with lead-203. In: Heavy Metals in theEnvironment (London: CEP Consultants).
Hodgson, S.A., Rance, E.R., Stradling, G.N., Hodgson, A., Fell, T.P., Youngman, M.J., Moody, J.C.,
Ansoborlo, E., 2000. Biokinetics of thorium dioxide and its decay products in the rat after
alveolar deposition: implications for human exposure. Chilton, NRPB-M1192.
Hodgson, S.A., Stradling, G.N., Hodgson, A., Smith, T.J., Youngman, M.J., Moody, J.C.,
Ansoborlo, E., 2003. Biokinetics and assessment of intake of thorium dioxide. Radiat. Prot.
Dosim. 105, 115–118.
Hong, Y.C., Yen, P.K.-J., Shaw, J.H., 1968. An analysis of the growth of the cranial vault in rabbits
by vital staining with lead acetate. Calc. Tiss. Res. 2, 271-285.
Hu, H., Milder, F.L., Burger, D.E., 1989. X-ray fluorescence: Issues surrounding the application of a
new tool for measuring burden of lead. Environ. Res. 49, 295-317.
Hursh, J. B.; Greenwood, M. R.; Clarkson, T. W.; Allen, J.; Demuth, S. (1980) The effect of ethanolon the fate of mercury vapor inhaled by man. J. Pharmacol. Exp. Ther. 214, 520-527.
Hursh, J.B., 1973. Retention of Pb-210 in beagle dogs. Health Phys. 25, 29-35.
Hursh, J.B., Brown, C., 1969. Tissue distribution of 212Bi in rats. Proc. Soc. Exp. Biol. Med. 131,
116-120.
Hursh, J.B., Mercer, T.T., 1970. Measurement of 212Pb loss rate from human lungs. J. Appl. Physiol
28, 268–274.
Hursh, J.B., Schraub, A., Sattler, E.L., Hofmann, H.P., 1969. Fate of 212Pb inhaled by humansubjects. Health Phys. 16, 257–267.
Hursh, J.B., Suomela, J., 1968. Absorption of Pb-212 from the gastrointestinal tract of man. Acta
Radiol. Ther. Phys. Biol. 7, 108-120.
Hursh, J.B.; Clarkson, T. W.; Cherian, M. G.; Vostal, J. J.; Mallie, R. V. (1976) Clearance of
mercury (Hg-197, Hg-203) vapor inhaled by human subjects. Arch. Environ. Health 31,
302-309.
ICRP 1994. Dose Coefficients for Intakes of Radionuclides by Workers, ICRP Publication 68. Ann.
ICRP 24(4).
ICRP 2002a. Basic anatomical and physiological data for use in radiological protection: Reference
values, ICRP Publication 89, Ann. ICRP 32(3/4).
ICRP 2002b. Guide for the Practical Application of the ICRP Human Respiratory Tract Model. ICRP
Supporting Guidance 3 Ann. of the ICRP 32(1–2).
ICRP, 1975. Report of the Task Group on Reference Man, ICRP Publication 23. Oxford, Pergamon
Press.
ICRP, 1980. Limits on Intakes of Radionuclides for Workers. ICRP Publication 30, Pt.2. Ann. ICRP
4(3/4).
ICRP, 1993. Age-dependent Doses to Members of the Public from Intake of Radionuclides: Part 2,
Ingestion dose coefficients. ICRP Publication 67. Ann. ICRP 23. (3/4).
Ishihara, N., Matsushiro, T., 1986. Biliary and urinary excretion of metals in humans. Arch. Environ.
Health 41, 324-330.
James, A.C., Greenhalgh, J.R., Smith, H., 1977. Clearance of lead-212 ions from rabbit bronchial
epithelium to blood. Phys. Med. Biol. 22, 932–948.
James, H., Hilburn, M., Blair, J., 1985. Effects of meal times on uptake of lead from thegastrointestinal tract in humans. Hum Toxicol., 4, 401-407.
Jeffrey M. R.; Freundlich, H. F.; Bailey, D. M. (1958). Distribution and excretion of radiogold inanimals. Ann. rheum. Dis. 17:52-60.

163

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6487
6488
6489
6490
6491
6492
6493
6494
6495
6496
6497
6498
6499
6500
6501
6502
6503
6504
6505
6506
6507
6508
6509
6510
6511
6512
6513
6514
6515
6516
6517
6518
6519
6520
6521
6522
6523
6524
6525
6526
6527
6528
6529
6530
6531
6532
6533
6534
6535
6536

Jellum, E.; Munthe, E.; Guldal, G.; Aaseth, J. (1980). Fate of the gold and the thiomalate part after
intramuscular administration of aurothiomalate to mice. Ann. Rheum. Dis. 39:155-158.
Johnson, J. E.; Johnson, J. A. (1968) A new value for the long component of the effective halfretention time of 203Hg in the human. Health Phys. 14, 265-266.
Jonsson, F.; Sandborgh-Englund, G.; Johanson, G. A. (1999) Compartmental model for the kinetics
of mercury vapor in humans. Toxicol. Appl. Pharmacol. 155, 161-168.
Joselow, M. M.; Goldwater, L. J.; Weinberg, S. B. (1967) Absorption and excretion of mercury inman. XI. Mercury content of “normal” human tissues. Arch. Environ. Health 15, 64-66.
Jugo, S. (1976) Retention and distribution of 203HgCl2 in suckling and adult rats. Health Phys. 30,
241-243.
Kalkwarf, D.R., Jackson, P.O., 1984. Lung-clearance classification of radionuclides in calcined
phosphate rock dust. PNL-5221, Richland, WA. Pacific Northwest Laboratory Reports.
Kalkwarf, D.R., Jackson, P.O., Hardin, J.M., 1984. Lung-clearance classification of radionuclides incoal fly ash. Health Phys. 47, 37–45.
Keller, C. A., Doherty, R. A. 1980. Distribution and excretion of lead in young and adult female
mice. Environ Res 21, 217-228.
Krahwinkel, W.; Herzog, H.; Feinendegen, L. E. (1988). Paramacokinetics of thallium-201 in normal
individuals after routine myocardial scintigraphy. J. Nucl. Med. 29:1582-1586.
Lacroix, P., 1960. Ca-45 autoradiography in the study of bone tissue. In: Bone as a tissue (Rodahl K,
Nicolson JT, Brown EM, Eds). New York, McGraw-Hill, pp. 262-279,
Lathrop, K. A.; Harper, P. V.; Gloria, I. V.; Rich, M. (1975). Intestinal localization of Tl-201. J.
Nucl. Med. 16:545.
Lathrop, K. A.; Tsui, B. M. W.; Chen, C.-T.; Harper, P. V. (1989). Multiparameter extratrapolationof biodistribution data between species. Health Phys. 57, Suppl. 1:121-126.
Lawrence, J. S. (1961). Studies with radioactive gold. Ann. Rheum. Dis. 20:341-352.
Leggett, R.W., 1993. An age-specific kinetic model of lead in humans. Environ. Health Perspect. 101,598-616.
Lie, R.; Thomas, R. G.; Scott, J. K. (1960). The distribution and excretion of thallium-204 in the rat,with suggested MPC’s and a bioassay procedure. Health Phys. 2:334-340.
Lindh, U., Brune, D., Nordberg, G., 1978. Microprobe analysis of lead in human femur by proton
induced x-ray emission (PIXE). Sci. Total Environ. 10, 31-37.
Lloyd, R.D., Mays, C.W., Atherton, D.R., Bruenger, F.W., 1975. 210Pb studies in beagles. HealthPhys. 28, 575-583.
MacDonald, N.S., Ezmirlian, F., Spain, P., McArthur, C., 1951. The ultimate site of skeletal
deposition of strontium and lead. J. Biol. Chem. 189, 387-399.
Mallon, R.P., 1983. A metabolic model of lead kinetics based upon measured organ burdens during
chronic exposure experiments with infant and juvenile baboons. Dissertation. New York
University.
Manton, W.I., Cook, J.D., 1984. High accuracy (stable isotope dilution) measurements of lead inserum and cerebrospinal fluid. Br. J. Ind. Med. 41, 313-319.
Marsh J.W., Gregoratto, D., Karcher, K., Nosske D., Bessa Y., Blanchardon E., Hofmann W.,
Tomasek, L., 2011. Dosimetric calculations for uranium miners for epidemiologicalstudies. Radiat. Prot. Dos. pp. 1-13, doi:10.1093/rpd/ncr310.
Marsh, J.W., Birchall, A., 1999. Determination of lung-to-blood absorption rates for lead and bismuththat are appropriate for radon progeny. Radiat. Prot. Dosim. 83, 331–337.
Martell, E.A., 1974. Radioactivity of tobacco trichomes and insoluble cigarette smoke particles.
Nature 249, 215-217.
Mascarenhas, B. R.; Granda, J. L.; Freyberg, R. H. (1972). Gold metabolism in patients withrheumatoid arthritis treated with gold compounds – reinvestigated. Arthritis andRheumatism 15:391-402.

164

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6537
6538
6539
6540
6541
6542
6543
6544
6545
6546
6547
6548
6549
6550
6551
6552
6553
6554
6555
6556
6557
6558
6559
6560
6561
6562
6563
6564
6565
6566
6567
6568
6569
6570
6571
6572
6573
6574
6575
6576
6577
6578
6579
6580
6581
6582
6583
6584
6585
6586
6587
6588

Massarella, J. W.; Pearlman, R. S. (1987). Gold disposition in the rat: Studies of its plasma half-lifeand its urinary, biliary and fecal elimination pathways. J. Pharmacol. Exp. Ther. 243:247257.
McQueen, E. G.; Dykes, P. W. (1969). Transport of gold in the body. Ann. Rheum. Dis. 28:437-442.
Miyake, M., Ishigaki, K., Suzuki, T., 1986. Structure refinements of Pb2+ ion-exchanged apatites by
x-ray powder pattern-fitting. J. Solid State Chem. 61, 230-235.
Moody, J.C., Davies, C.P., Stradling, G.N., 1994a. Biokinetics of thorium and daughter radionuclides
after deposition in the rat lung as fluoride and hydroxide. In: Mohr, U., Dungworth, D.L.,
Mauderly, J.L., Oberdörster, G. (Eds.), Proc. Fourth International Inhalation Symposium,
Hannover, March 1–5, 1993. Toxic and Carcinogenic Effects of Solid Particles in the
Respiratory System, pp. 611–614.
Moody, J.C., Stradling, G.N., 1992. Biokinetics of thorium and daughter radionuclides after
deposition in the rat lung. J. Aerosol Sci. 23, S523–S526.
Moody, J.C., Stradling, G.N., Pearce, M.J., Gray, S.A., 1994b. Biokinetics of Thorium and Daughter
Radionuclides after Deposition in the Rat Lung as Nitrate: Implications for Human
Exposure. NRPB-M525, Chilton, UK.
Morgan, A., Holmes, A., Evans, J.C., 1977. Retention, distribution, and excretion of lead by the rat
after intravenous injection. Br. J. Ind. Med. 34, 37-42.
Morrow, P.E., Better, F., Amato, F., Gibb, F.R., 1980. Pulmonary retention of lead: an experimental
study in man. Environ. Res. 21 373–384.
Nakamura, K.; Nishiguchi, I.; Takagi, Y.; Kubo, A.; Hashimoto, S. (1985). Distribution of 201Tl inblood. Radioisotopes. 34:550-554.
Newton, D.; Fry, F. A. (1978) The retention and distribution of radioactive mercuric oxide following
accidental inhalation. Ann. Occup. Hyg. 21, 21-32.
Potter, G. D.; Vattuone, G. M.; McIntyre, D. R. (1971). The fate and implications of ingested 204Tl
in a dairy cow and a calf. Health Phys. 20:657-662.
Rabinowitz, M. B., Wetherill, G.W., Kopple, J.D., 1974. Studies of human lead metabolism by use of
stable isotope tracers. Environ. Health Perspect. 5-7, 145-153.
Rabinowitz, M.B., Wetherill, G.W., Kopple, J.D., 1973. Lead metabolism in the normal human:
Stable isotope studies. Science 182, 725-727.
Rabinowitz, M.B., Wetherill, G.W., Kopple, J.D., 1976. Kinetic analysis of lead metabolism inhealthy humans. J. Clin. Invest 58, 260-270.
Rendall, R.E.G., Baily, P., Soskolne, C. L., 1975. The effect of particle size on absorption of inhaledlead. Am. Ind. Hyg. Assoc. J. 36, 207–213.
Rhoads, K., Sanders, C.L., 1985. Lung clearance, translocation, and acute toxicity of arsenic,
beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium oxides following
deposition in rat lung. Environ. Res. 36, 359–378.
Rothstein, A.; Hayes, A. D. (1960) The metabolism of mercury in the rat studied by isotope
techniques. J. Pharmacol. Exp. Ther. 130, 166-176.
Rubin, M.; Sliwinski, A.; Photias, M,; Feldman, M.; Zvaifler, N. (1967). Influence of chelation ongold metabolism in rats. Proc. Soc. Exp. Biol. Med. 124:290-296.
Scheiman-Tagger, E., Brodie, A.G., 1964. Lead acetate as a marker of growing calcified tissues.
Anat. Rec. 150, 435-440.
Silva, A. J.; Fleshman, D. G.; Shore, B. (1973). The effects of penicillamine on the body burdens ofseveral heavy metals. Health Phys. 24:535-539.
Singh, N.P., Bennett, D.B., Wrenn, M.E., 1986. Concentrations of 210Pb and its states of equilibriumwith 238U, 234U, and 230Th in U miners' lungs. Health Phys., 51, 501–507.
Stradling, G.N., Davies, C.P., Moody, J.C., Gray, S.A., Wilson, I., Ellender, M., 2005. Biokinetics ofthorium and daughter radionuclides after deposition as fluoride and hydroxide in the rat
lung: implications for occupational exposure. NRPB-DA/05/2005, Chilton, UK.
Strauss, H. W.; Harrison, K.; Langan, J. K.; Lebowitz, E.; Pitt, B. (1975). Thallium-201 formyocardial imaging. Circulation 51:641-645.

165

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6589
6590
6591
6592
6593
6594
6595
6596
6597
6598
6599
6600
6601
6602
6603
6604
6605
6606
6607
6608
6609
6610
6611
6612
6613

Sugawa-Katayama, Y.; Koishi, H.; Danbara, H. (1975). Accumulation of gold in various organs ofmice injected with gold thioglucose. J. Nutr. 105:957-962.
Suzuki, M.; Morikawa, M.; Tomita, K.; Yoshida, A.; Suwo, M.; Matsushima, H.; Kato, M.; Ueda, N.;
Yamada, H.; Hazue, M. (1978). Thallous chloride-201Tl – Fundamental studies on its
behavior and clinical evaluation. Kaku Igaku. Japanese J. Nucl. Med. 15:27-40.
Tipton, I.H., Cook, M.J., 1963. Trace elements in human tissue. Part II. Adult subjects from theUnited States. Health Phys. 9, 103-145.
Vander, A.J., Taylor, D.L., Kalitis, K., Mouw, D.R., Victery, W., 1977. Renal handling of lead in
dogs: Clearance studies. Am. J. Physiol. 233, F532-F538.
Verbeeck, R.M., Lassuyt, C.J., Heijligers, H.J., Driessens, F.C., Vrolijk, J.W., 1981. Lattice
parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite.
Calc. Tiss. Int. 33, 243-247.
Victery, W., Vander, A.J., Mouw, D.R., 1979. Renal handling of lead in dogs, stop-flow analysis.
Am. J. Physiol. 237, F408-F414.
Vincent, J., 1957. Les remaniements de l'os compact marque a l'adie de plomb. Revue Belge de Path.
et Med. Exper. 26, 168-172.
Wells, A.C., Venn, J.B., Heard, M.J., 1975. Deposition in the lung and uptake to blood of motor
exhaust labelled with Pb-203. In: Walton, W.H., McGovern, B. (Eds.), Inhaled Particles IV,
pp. 175-189. Proceedings of a Symposium of the British Occupational Hygiene Society,
Edinburgh.
Yen, P. K., Shaw, J. H. 1977. Remodeling of compact bone studied with lead acetate as an intravitalstain. J Dent. Res. 56, 961-966.

166

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6614
6615
6616
6617
6618
6619
6620
6621
6622
6623
6624
6625
6626
6627

10.
10.1.

Chemical forms in the workplace(479) Bismuth is a metalloid which mainly occurs in oxidation state III. Arsenic andantimony are good chemical analogues of bismuth. Bismuth is encountered in industry in avariety of chemical and physical forms, including oxides, chlorides, fluorides, iodides, andsulphides.
(480) Several isotopes of bismuth with short half-lives occur within the radioactive
disintegration chains of actinium, radium and thorium.
Table 10-1. Isotopes of bismuth addressed in this report
Isotope
Bi-200Bi-201
Bi-202
Bi-203
Bi-204
Bi-205
Bi-206
Bi-207
Bi-208Bi-210a
Bi-210m
Bi-212
Bi-213
Bi-214a

6628
6629
6630
6631
6632
6633
6634
6635
6636
6637
6638
6639
6640
6641
6642
6643
6644
6645
6646
6647

BISMUTH (Z = 83)

a

10.2.

Physical half-life
36.4 m108 m
1.72 h
11.76 h11.22 h15.31 d6.243 d32.9 y3.68E+5 y
5.013 d3.04E+6 y60.55 m45.59 m19.9 mDecay mode
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+
EC, B+
EC
B-, A
A
B-, A
B-, A
B-, A

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides
are given on accompanying electronic disk.

Routes of Intake

10.2.1. Inhalation
Absorption Types and parameter values(481) Very little information from which parameter values can be assessed is available
from experimental studies of the behaviour of bismuth deposited in the respiratory tract.
(482) Absorption parameter values and Types, and associated fA values for particulate
forms of bismuth are given in Table 10-2. For radiation protection purposes, the mostimportant exposures to radioisotopes of bismuth are as decay products of radon. Dose
coefficients for isotopes of bismuth inhaled as radon decay products are given in the radon
section, where factors such as the relevant aerosol size distribution are addressed. Otherwise,
exposures to radioisotopes of bismuth occur most often as decay products associated withintakes of uranium, thorium or radium.
(a) Bismuth as a decay product of radon(483) In this section studies are considered in which 212Bi (half-life 61 minutes) formed

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6648
6649
6650
6651
6652
6653
6654
6655
6656
6657
6658
6659
6660
6661
6662
6663
6664
6665
6666
6667
6668
6669
6670
6671
6672
6673
6674
6675
6676
6677
6678
6679
6680
6681
6682
6683
6684
6685
6686
6687
6688
6689
6690
6691
6692
6693
6694
6695

from decay of 220Rn (half-life 56 seconds) 216Po (half-life 0.15 seconds) and 212Pb (half-life
11 hours), or 214Bi (half-life 20 minutes) formed from decay of 222Rn (half-life 3.8 days),218
Po (half-life 3.1 minutes) and 214Pb (half-life 27 minutes) was inhaled directly, while still
airborne. For decay schemes, see the thorium and uranium sections. Studies in which bismuthions were administered to the respiratory tract in a liquid medium, which might also be
relevant to bismuth as a decay product of radon, are considered below in the section on
particulate forms.
(484) Drew (1971) reported that the tissue distributions of 212Pb and 212Bi activities weresimilar in rats following exposure to 220Rn (thoron) and its decay products for 2 days.
However, the exposure situation was complex, because the 212Pb and 212Bi in tissues
originated from inhalation of 220Rn and its decay within the body, inhalation of 212Pb and212
Bi, and also their ingestion from food and preening of fur. It is therefore difficult toestimate how much of the 212Bi originated from intake of 212Bi, and how much from decay of212
Pb in the body.
(485) Butterweck et al. (2001, 2002) carried out volunteer experiments to determine theabsorption rate of unattached radon progeny. (For further information see the lead inhalation
section.) Volunteers inhaled an aerosol which was predominantly unattached radon progeny.
Measurements were made of 222Rn, 214Pb and 214Bi in blood samples taken at the end of a 30minute exposure (Butterweck et al., 2002). In vivo measurements of the head and chest werecarried out over a 30-minute period, starting approximately 7 minutes after exposure(Butterweck et al., 2001). No clearance from the head (other than physical decay) was
observed over this period for 214Pb, indicating that a small fraction of the unattached 214Pb
was absorbed rapidly to blood (sr >> 100 d–1), as measured by the blood sample, while therest (fraction fb) was bound to tissues (or stationary mucus). Assuming a rapid dissolution
rate (sr) of 1000 d–1 with fr=1.0 and an uptake rate from the bound state (sb) of 1.7 d–1,
Butterweck et al. (2002) estimated values of fb in the range 0.7–0.85, for radon progeny(without distinguishing between 214Pb and 214Bi) from the blood measurements. However,
Butterweck et al. (2002) also estimated “absorption rates” for 214Pb and 214Bi from theiractivities in the blood sample and the estimated respiratory tract deposition, assuming thatabsorption from respiratory tract to blood could be represented by a single rate constant (sr)i.e. fr =1 and fb =0, although this model seems inconsistent with the in vivo measurements.
They obtained absorption half-times of ~60 minutes for 214Pb and ~25 minutes for 214Bi,
suggesting that there was greater absorption of 214Bi than of 214Pb by the end of the exposure
when the blood sample was taken.
(486) Hursh et al. (1969) followed lung retention, blood concentration, urinary and fecal
excretion of 212Pb in ten volunteers for up to 3 d after inhalation (by mouth) of an aerosol
formed by mixing 212Pb (formed from decay of 220Rn/216Po) with natural room aerosol. (Forfurther information see the lead inhalation section.) Measurements of 212Bi were also made,but because of its short half-life fecal excretion of 212Bi could not be determined. Initialdeposition of 212Bi in the lungs was ~10% of the 212Pb activity, as expected because of its
lower concentration in the air. Measurements of urinary excretion of 212Bi were reported forone subject. Hursh and Mercer (1970) measured 212Bi activities in blood and urine in fourvolunteers after inhalation of an aerosol formed by mixing 212Pb with natural room aerosol.
(For further information see the lead inhalation section). However, the results were notreported “to conserve space and because the findings were in all cases similar to thosereported earlier” with reference to Hursh et al. (1969). Marsh and Birchall (1999) used themeasurements of urinary excretion of 212Bi reported by Hursh et al. (1969) to estimate theabsorption rate for bismuth. They took account of ingrowth from decay of its parent 212Pb in
168

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6697
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6700
6701
6702
6703
6704
6705
6706
6707
6708
6709
6710
6711
6712
6713
6714
6715
6716
6717
6718
6719
6720
6721
6722
6723
6724
6725
6726
6727
6728
6729
6730
6731
6732
6733
6734
6735
6736
6737
6738
6739
6740
6741
6742
6743

the lungs and following systemic uptake. They assumed that absorption of both lead andbismuth could be represented by a single component i.e. fr = 1 and fb = 0. In the analysis theabsorption half-time for lead was fixed at 10 hours. The best fit was obtained with anabsorption half-time for bismuth of 13 hours, suggesting Type F behaviour. However, theauthors noted that this value should be treated with caution as it was based on data from asingle subject. A more detailed analysis of the results of human volunteer studies of inhaledradon progeny was carried out here (i.e. by the Task Groups), to estimate absorption
parameter values appropriate for short-lived radon progeny, giving specific consideration to
the rapid absorption phase and binding. (For further information see the lead inhalation
section.) However, for the study by Hursh et al. (1969) the information available did not
permit assessment of fb.
(b) Particulate aerosols(487) In all of the studies summarised below, except that of Greenhalgh et al. (1977) who
administered 207BiCl3, isotopes of uranium or thorium with their decay products wereadministered by intratracheal instillation into rats, and measurements were made of the lungretention and tissue distribution of 228Th, 212Pb, 212Bi and 208Tl at times from 6 or 24 hours
onwards. In all these studies the distributions of 212Bi (and 208Tl) were similar to those of theparent 212Pb. Because their physical half-lives are so short (61 minutes and 3 minutes
respectively) measurements made at 6 hours onwards would be mainly of activity formed
from decay of 212Pb within the body, rather than from intake of 212Bi. The similar
distributions of 212Bi and 208Tl (allowing for the 36% branching ratio for the formation of208
Tl from decay of 212Bi) to those of 212Pb might suggest that there was not rapid movementof 212Bi from the site (e.g. the lungs) in which it was formed by decay of 212Pb. However,212
Bi (and 208Tl) would have grown in rapidly between dissection of the animals andmeasurements of activities in tissues. Thus the activities of 212Bi (and 208Tl) measured may
have been significantly higher than those present in vivo, and without detailed information(which is not available) about the time which elapsed between dissection of the animals andmeasurements, it is not possible to correct for this and hence estimate the absorption rate of
the bismuth from the respiratory tract.
Bismuth chloride (BiCl3)(488) Greenhalgh et al. (1977) followed the lung retention of 207Bi for about an hour after
instillation of 207Bi instilled as BiCl3 solution into the bronchi of rabbits. There was little
clearance in this time and the amount of 207Bi in blood after 90 minutes was <1% of that
instilled. The authors estimated that the clearance half-time was greater than 1 day. Thisappears to have been a pilot study that was not followed up.
Bismuth nitrate (Bi(NO3)3)(489) Ballou et al. (1986) measured lung retention and tissue distribution of 232U, 228Th,
224
Ra, 212Pb, 212Bi and 208Tl at 24 hours after intratracheal instillation into rats of 232U nitratewith its decay products. (For further information, see the uranium inhalation section.) Moody
et al. (1994a; Moody and Stradling, 1992) measured the tissue distribution of 228Th, 212Pb,
212
Bi and 208Tl, at times from 6 hours to 7 days after intratracheal instillation into rats of anitrate solution of 228Th in equilibrium with its decay products. (For further information, see
the thorium and lead inhalation sections.) In both studies the distributions of 212Bi (and 208Tl)
were similar to those of 212Pb. However, no estimate could be made by the task group of therate of absorption of the 212Bi from the lungs (see above).
169

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6744
6745
6746
6747
6748
6749
6750
6751
6752
6753
6754
6755
6756
6757
6758
6759
6760
6761
6762
6763
6764
6765
6766
6767
6768
6769
6770
6771
6772
6773
6774
6775
6776
6777
6778
6779
6780
6781
6782
6783
6784
6785
6786
6787
6788
6789
6790
6791

Bismuth hydroxide (Bi(OH)3)(490) Moody et al. (1994b; Stradling et al., 2005) measured the tissue distributions of
228
Th, 212Pb, 212Bi and 208Tl, at times from 1 to 28 days after intratracheal instillation into ratsof a suspension of 228Th hydroxide in equilibrium with its decay products. (For further
information, see the thorium and lead inhalation sections.) The distributions of 212Bi (and208
Tl) were similar to those of 212Pb. However, no estimate could be made here of the rate ofabsorption of the 212Bi from the lungs (see above).
Bismuth fluoride (BiCl3)(491) Moody et al. (1994b; Stradling et al., 2005) measured the tissue distributions of
228
Th, 212Pb, 212Bi and 208Tl, at times from 1 to 28 days after intratracheal instillation into ratsof a suspension of 228Th fluoride in equilibrium with its decay products. (For further
information, see the thorium and lead inhalation sections.) The distributions of 212Bi (and208
Tl) were similar to those of 212Pb. However, no estimate could be made here of the rate ofabsorption of the 212Bi from the lungs (see above).
Thorium dioxide(492) Hodgson et al. (2000, 2003) measured the tissue distributions of 228Th, 212Pb, 212Bi
and 208Tl, at times from 1 to 168 days after intratracheal instillation into rats of suspensions of
232
Th dioxide enriched with 228Th, in equilibrium with its decay products. (For further
information, see the thorium and lead inhalation sections.) There was little absorption of thethorium itself, consistent with assignment to Type S. The activity of 212Pb in the lungs was
lower than of that of the thorium, which was attributed to diffusion of 220Rn (thoron) andrecoil of the progeny from alpha particle decay. The distributions of 212Bi (and 208Tl) weresimilar to those of 212Pb. However, no estimate could be made here of the rate of absorptionof the 212Bi from the lungs (see above).
Decay products of bismuth formed in the respiratory tract(493) The general approach to treatment of decay products formed in the respiratory tract
is described in Part 1, Section 3.2.3. In summary, it is expected that generally the rate at
which a particle dissociates is determined by its matrix, and hence the physico-chemical formof the inhaled material. It is recognised that nuclei formed by alpha decay within a particle
matrix may be expelled from it into the surrounding medium by recoil, but to implement thisroutinely would add greatly to the complexity of calculations. It is expected that the behaviourof soluble (e.g. Type F) material in the respiratory tract would depend on its elemental form,
i.e. that of the decay product. Nevertheless, for simplicity, in this series of documents theabsorption parameter values of the parent are, by default, applied to all members of the decay
chain formed in the respiratory tract. Exceptions are made for noble gases formed as decay
products, which are assumed to escape from the body directly, at a rate of 100 d–1, in addition
to other routes of removal.
(494) For decay schemes of bismuth isotopes in the natural decay series: 210Bi, 211Bi, 212Bi,
and 214Bi, see the uranium and thorium sections. Studies specifically comparing the behaviourof bismuth with that of its decay product (thallium) are summarised here.
(495) As noted above, measurements have been made of the tissue distributions of 212Bi
and its decay product, 208Tl, following administration to rats of 228Th in various chemical
forms (nitrate, hydroxide, fluoride, dioxide), in equilibrium with its decay products. In allthese studies the distributions of 212Bi (and 208Tl) were similar to each other and those of the170

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
6792
6793
6794
6795
6796
6797
6798
6799
6800
6801
6802
6803
6804
6805
6806
6807
6808
6809
6810
6811
6812
6813
6814
6815
6816
6817
6818
6819
6820
6821
6822
6823
6824
6825

parent 212Pb. Because their physical half-lives are so short (61 minutes and 3 minutes
respectively) measurements made at 6 hours onwards would be mainly of activity formed
from decay of 212Pb within the body, rather than from intake of 212Bi (or 208Tl). However, thehalf-life of 208Tl (3 minutes) is so short that it would easily reach equilibrium with 212Bi
between dissection of the animals and measurements of activities in tissues. It is not possible
to correct for this ingrowth and hence estimate the absorption rate from the respiratory tract of
the thallium formed as a decay product of bismuth. However, since the half-life of 208Tl is so
short (as is that of 207Tl present in the 235U decay series, 5 minutes), the absorption rate would
have to be very high to influence dose assessments.
Rapid dissolution rate for bismuth(496) Inferences drawn from the three studies outlined above, which might provide
information on the rapid dissolution rate for bismuth, are contradictory. Greenhalgh et al.
(1977) estimated that the lung retention half-time was greater than 1 day following instillationof 207BiCl3 into the bronchi of rabbits: much slower absorption than that of lead over theperiod (one hour) of measurement. Marsh and Birchall (1999) estimated the absorption rate
for bismuth using measurements of urinary excretion of 212Bi by a volunteer following
inhalation of attached radon decay products reported by Hursh et al. (1969). They assumed
that absorption of both lead and bismuth could be represented by a single component i.e. fr =1 and fb = 0. The best fit was obtained with an absorption half-time for bismuth of 13 hours,
very similar to that obtained for lead, i.e. sr ~1 d–1. Butterweck et al. (2002) assessed thatabsorption of 214Bi was faster than that of 214Pb during inhalation of unattached radon
progeny.
(497) The main use for absorption parameter values for bismuth is in assessing doses frominhaled radon decay products. A value of sr of 1 d–1, based on the assessment of Marsh andBirchall (1999) is adopted here. The short-lived isotopes of bismuth (214Bi, 212Bi and 211Bi)
formed as a decay product of radon have radioactive decay constants >> 1 d-1, so the bismuth
absorption rate will have little influence in assessing doses from inhaled radon decay
products.
Extent of binding of bismuth to the respiratory tract(498) There is insufficient information to estimate the extent of any bound state. It istherefore assumed by default that fb = 0.

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Table 10-2. Absorption parameter values for inhaled and ingested bismuth

6826
6827

Absorption
parameter Absorption fromvaluesathealimentary–1–1frsr (d ) ss (d ) tract, fA

Inhaled particulate materials
Default parameter valuesc
Absorption
Assigned forms
TypeF
Bismuth as a decay product 1
of radonM
All unspecified formsd
0.2
—
S
0.01
Ingested material
All forms
6828
6829
6830
6831
6832
6833
6834
6835
6836
6837
6838
6839
6840
6841
6842
6843
6844
6845
6846
6847
6848
6849
6850
6851
6852
6853
6854
6855
6856
6857
6858
6859
6860
6861
6862

1

–

0.05

1
1

0.005
1x10-40.01
5x10-40.05

a

It is assumed that for bismuth the bound state can be neglected, i.e. fb = 0. The values of sr for Type F, M and
S forms of bismuth (1 d–1) are element-specific.
b
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type (or specific value where given) and the fA value for ingested soluble forms of bismuth (0.05).
cMaterials (e.g. bismuth as a decay product of radon) are listed here where there is sufficient information toassign to a default absorption Type, but not to give specific parameter values (see text).
dDefault Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

10.2.2. Ingestion(499) There are few available data on bismuth absorption in human and animals. It has
been stated that basic salts of bismuth are only poorly absorbed from the gastrointestinal tract(Sollman, 1957) and suggested that the fractional absorption of dietary bismuth from thegastrointestinal tract is about 0.08 (ICRP, 1975).
(500) The absorption of bismuth from five 205Bi compounds was studied in man (Dresow
at al., 1992). From single oral doses of these five compounds, less than 0.1% bismuth wasabsorbed and excreted in the urine, with a significantly higher absorption from the colloidal
subcitrate and gallate compounds (about 0.04%) than from salicylate, nitrate and aluminate(0.002 to 0.005%). Koch et al. have studied the pharmacokinetics of bismuth following
administration of single or multiple oral doses of ranitidine bismuth citrate to healthy subjects(Koch et al., 1996a,b). They showed that bismuth absorption from ranitidine bismuth citrate
was below 0.5% of the dose, and bismuth elimination was predominantly by renal secretion.
Boertz et al. (2009) studied the biotransformation and excretion of bismuth after ingestion of
215 mg of colloidal bismuth subcitrate by 20 male volunteers. Bismuth absorption in thestomach and upper intestine was very low, and a total of 0.03 to 1.2% of the ingested Bi was
eliminated in the urine during the 56 hours test.
(501) The bioavailability of 205Bi from various oral bismuth preparations was also studied
in rats (Dresow et al., 1991). The intestinal absorption, calculated from 205Bi whole bodyretention and accumulated urinary excretion was very low, but significantly higher (about0.3%) from bismuth citrates (Bi citrate and colloidal Bi subcitrate) as compared to bismuth
nitrate, salicylate, gallate and alluminate (0.04 to 0.11%).
(502) The ICRP Publication 30 recommended an absorption value of 0.05 to apply to all172

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6901
6902
6903
6904
6905
6906
6907
6908
6909
6910

chemical forms (ICRP, 1980).
(503) The most recent studies confirm this absorption value for bismuth and an fA of 0.05
is therefore adopted here for direct ingestion of all chemical forms.
10.2.3. Systemic Distribution, Retention and Excretion
10.2.3.1. Summary of the database(504) Bismuth has been used since the late 1700s as a therapeutic agent for a number ofdisorders of the human body. For example, it has been used externally on burns and inflamedskin; orally for gastrointestinal inflammations, ulcers, and as an opaque medium for x-ray
examinations; and intramuscularly for treatment for syphilis (Sollman, 1957). Serious
adverse affects including death have sometimes occurred. Successful treatments often have
involved maintenance of maximal nontoxic concentrations of bismuth. The optimal dosages
have been worked out by measurement and estimation of absorption, distribution, andexcretion, both clinically and in animal studies.
(505) The systemic biokinetics of bismuth has been found to vary with the route ofadministration and the form administered. Concentration of particulate or colloidal forms isparticularly high in the reticuloendothelial (RE) system (Eridani et al., 1964; Einhorn et al.,1964).
(506) In the early period after acute input to blood, most forms of bismuth are rapidly
cleared from plasma to extracellular fluids and excretion pathways. For example, 75% ormore of bismuth in human plasma intravenously injected into rats or bismuth citrate
intravenously injected into humans left the circulation in the first 5-10 min (Hursh and
Brown, 1969; Coenegracht and Dorleyn, 1961; Newton et al., 2001). After the rapid
equilibration between blood plasma and extracellular fluids the disappearance of bismuth
from blood is much slower. In a human subject receiving 207Bi citrate by intravenous
injection, about 6% of the injected amount remained in blood after 1 h, 1% after 7 h, and
0.5% after 1 d (Newton et al., 2001).
(507) Data on the distribution of bismuth in blood are inconsistent. Some investigators
have concluded that bismuth shows little affinity for erythrocytes (Benet, 1991; Koch et al.,1996a), while others have concluded that bismuth in blood is present primarily in erythrocytes(D’Souza and Francis, 1987; Rao and Feldman, 1990; Newton et al., 2001).
(508) In studies involving continued oral dosing of human subjects for 6-8 weeks withbismuth compounds, there was a continual rise in plasma concentration and the urinary
excretion rate (Froomes et al., 1989). Apparent steady-state levels were reached after about
18 days (range 7-29 days). Renal clearance of bismuth from normal volunteers and gastritis
patients averaged 22.2 ml/min. Elimination half-lives based on declining concentrations ofbismuth in plasma and urine were 20.7 and 21.6 days, respectively. Similarly, in patients withbismuth encephalopathy, Boiteau et al. (1976) found plasma elimination half-times of about
13-22 days and urine half-times of about 10-20 days. Data of Loiseau and coworkers (1976)
indicated a half-time in plasma of about 23 days.
(509) The pharmacokinetics of bismuth was studied in 60 healthy male subjects, ages 1940 y, for single oral administration of ranitidine bismuth citrate and for twice daily doses for
28 days in 27 healthy male subjects, ages 20-49 y (Koch et al., 1996a,b). After single
administration the concentration of bismuth in plasma typically peaked after 30-45 min anddeclined with a half-time initially on the order of 1 h. The bismuth concentrations in plasma
for 15 subjects measured up to 154 d after the last intake indicated three components of173

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6954
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6958

removal with average half-times of 20 min, 11.1 h, and 20.7 d.
(510) Gavey et al. (1989) measured the bismuth concentration in plasma and urine in ninepatients before, during, and after treatment with tripotassium dicitrato bismuthate for six
weeks. The 24-h urinary clearance of bismuth was estimated as 19.4 and 19.8 plasma
volumes per day based on data for 3 and 6 weeks after the start of exposure, assuming aplasma volume of 3000 ml.
(511) Most forms of bismuth show high deposition in the kidneys and subsequent
clearance to urine (Durbin, 1960; Eridani et al., 1964; Matthews et al., 1964; Russ et al.,
1975; Pieri and Wegmann, 1981; Slikkerveer and de Wolff, 1989). Human subjects injectedwith bismuth citrate excreted a third or more of the administered bismuth in urine during thefirst day (Coenegracht and Dorleyn, 1961; Newton et al., 2001). Lower excretion rates havebeen observed for some forms used in clinical studies. For example, about 13% of bismuth
injected as citrate adsorbed on charcoal was excreted in urine during the first day(Coenegracht and Dorleyn, 1961), 2-3% of bismuth injected as phosphate appeared in urine
the first day (Coenegracht and Dorleyn, 1961), and as little as 5% of bismuth injected as a
salicylate suspension is excreted in urine during the first 3 wk after injection (Sollmann,
1957). Microscopic studies of the epithelium of the proximal renal tubules have shown
accumulations of bismuth in the nucleus, cytoplasm, and possibly the lysosomes (Slikkerveer
and de Wolff, 1989).
(512) Clinical data indicate that fecal excretion constitutes 4-10% of total excretion of
bismuth with oil solutions, 6-22% with "watery" solutions, and 12% with oil suspensions(Sollmann, 1957). In rats and rabbits, fecal excretion arising to a large extent from biliary
secretion accounts for 10-20% of the total excretion of bismuth (Pieri and Wegmann, 1981;
Vienet et al., 1983, Gregus and Klaassen, 1986).
(513) In a study of the fate of intravenously injected tracer doses of 206Bi in humansubjects, Coenegracht and Dorleyn (1961) concluded from in vivo measurements that 206Bi
injected as citrate was taken up and retained to a large extent by the liver and spleen. Theysuggested that injected bismuth citrate may form complexes with plasma proteins and that thesize of the bismuth protein complexes will largely determine the initial distribution of
bismuth in the body. A high rate of urinary excretion of 206Bi in the first few days after
injection presumably represented activity that did not attach to plasma proteins or was
released fairly quickly from these proteins.
(514) Extended retention of a portion of the administered bismuth has been reported for
relatively insoluble bismuth compounds used in clinical applications (Sollmann, 1957).
Autopsy measurements have been interpreted as indicating that the total bismuth stored in the
body for an extended period may be as much as 7% of the administered amount (Sollmann,
1957), with approximate relative concentrations (wet weight) of bismuth in different organs
being as follows: kidney, 33; liver, 6.8; spleen, 1.6; colon, 1.3; lung, 0.9; brain, 0.6; andblood, 0.5 (Sollmann and Seifter, 1942). The kidneys and liver each contained nearly 10% of
the total found in the body (Sollman, 1957).
(515) Buijs and coworkers (1985) found 207Bi (T1/2 = 38 y) remaining in two humansubjects treated a quarter century earlier with 206Bi injections contaminated with small
amounts of 207Bi. They estimated from measurements of the rate of decline of total-body
207
Bi and from assumptions on the early rate of excretion of bismuth that 7% of injectedbismuth is retained with a half-time close to 20 y. Buijs's estimate applies to bismuth injected
as phosphate or as citrate adsorbed on charcoal, the two forms known to be administered to atleast one of the subjects. These two forms are taken up to some extent by the RE system(Coenegracht and Dorleyn, 1961), and it appeared from external measurements that the long174

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6991
6992
6993
6994
6995
6996
6997
6998
6999
7000
7001
7002
7003
7004
7005

retained activity in the two human subjects was associated largely with organs of this system(Buijs et al., 1985).
(516) Newton et al. (2001) studied the biokinetics of bismuth in a healthy male volunteer
after intravenous injection with 207Bi citrate. They estimated that the liver contained 60% of
the body content at 3 d. An estimated 55% was lost in excreta, primarily urine, during the first
47 h. Longer-term losses were much slower. Approximately 0.6% of the injected amountremained at 924 d. The long-term half-time was estimated as 1.9 y.
(517) Studies on rats indicate elevated deposition in the kidneys and sometimes in theliver, but the systemic distribution varies with the form of bismuth reaching blood. For
example, the ratio of the concentration in the kidneys to that in the liver averaged roughly 15
at 2 h after intravenous (iv) injection with bismuth nitrate (Gregus and Klaassen, 1986); 10 at
2 h after iv injection of bismuth in human plasma (Hursh and Brown, 1969); 5 at 2-48 h afteriv injection with bismuth citrate (Pieri and Wegmann, 1981); 50 at 6-48 h after intraperitoneal
injection with bismuth citrate (Russ et al., 1975); 20 at 72-144 h after iv injection withbismuth nitrate (Vienet et al., 1983); and 40 at 2-6 h after intraperitoneal injection of bismuth
in a carbonate buffer (Zidenberg-Cherr et al., 1987).
(518) In studies on rabbits, the liver was generally a more important repository for bismuththan the kidneys (van den Werff, 1965). The systemic distribution of 206Bi was determinedfrom a few days up to about 2 wk after intravenous administration of different forms,
including citrate or phosphate in 5% charcoal suspension in saline, nitrate, phosphate in 5%
glucose, and acetate in saline solution. Distributions varied considerably from one form of206
Bi to another. As averages over all animals studied, all forms of 206Bi administered, and allobservation times, the liver, kidneys, skeleton, and remaining tissues contained about 38%,
18%, 17%, and 22%, respectively, of the body burden. Typically, the portion of the total-bodycontent in the skeleton increased with time while the portions in liver and kidneys decreased
with time.
(519) Deposition of bismuth in bone has also been observed in rats (Eridani et al., 1964;
Hursh and Brown, 1969; Russ et al., 1975; Gaucher et al., 1979; Gregus and Klaassen, 1986).
Reported values for uptake and retention by bone are highly variable and may depend on theadministered form of bismuth. At 4 d after intramuscular injection of 206Bi into rats as BiOCl
or BiO(OH), 14.4% of the administered dosage was found in the kidneys, 6.6% in liver, 1.5%
in bone, and 0.6% in muscle (Durbin, 1960). About three-fourths of the administered activity
was excreted in the first four days, mainly in urine. In rats receiving 206Bi citrate by
intraperitoneal injection, total-body activity declined from about 59% of the administeredactivity at 6 h to about 12-18% at 3-5 d (Russ et al., 1975). Bone contained about 4-7% of theadministered amount at 0.5 h and roughly 1% from 1 to 6 d. The kidney content declined
from almost 40% of the administered amount at 0.5 h to roughly 12% at 3-6 d. The liver
content was <1% of the administered amount from 0-6 d.
(520) Data for dogs injected with 224Ra (Lloyd et al., 1982) or 228Th indicate that there isconsiderable migration of 212Bi (T1/2 = 60.6 min) from its parent, 212Pb, in bone surfaces, redblood cells, and some soft tissues, and that much of the migrating bismuth accumulates in thekidneys or is quickly eliminated in urine. In human subjects who inhaled 212Pb, 212Bi escaped
more quickly from red blood cells than did its parent 212Pb, and the rate of urinary excretionof 212Bi was 3-4 times that of 212Pb (Hursh et al, 1969). In bone, 210Bi tends to remain to alarge extent with 210Pb at times remote from exposure, indicating that bismuth probably does
not readily escape from Pb in bone volume.

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7015
7016
7017
7018
7019
7020
7021
7022
7023

7024
7025
7026
7027

10.2.3.2. Systemic model(521) The structure of the biokinetic model for systemic bismuth is shown in Figure 10-1.
Transfer coefficients are listed in Table 10-3.
(522) It is assumed that bismuth leaves blood plasma at the rate 400 d-1 (half-time of
approximately 2.5 min) with three-fourths moving to the fast-turnover soft-tissuecompartment ST0 representing extracellular fluids in the present model. Outflow of theremaining one-fourth is divided as follows: 20% to urinary bladder contents, 4% to thecontents of the right colon, 30% to liver (compartment Liver 0), 30% to the urinary path, 5%
to other kidney tissue, 5% to bone surfaces, 0.5% to RBC, 1.3% to the slow-turnover softtissue compartment ST2, and the remaining 4.2% to the intermediate-term soft-tissuecompartment ST1. Half the activity deposited on bone surfaces is assigned to cortical boneand half to trabecular bone. The following removal half-times are assigned: 15 min from ST0
to plasma; 2 d from Liver 0, with 60% moving to the small intestine contents in bile and 40%
moving to Liver 1; 10 d from Liver 1 to Plasma; 1 d from the urinary path to urinary bladdercontents; 5 d from other kidney tissue to Plasma; 20 d from bone surface or ST1 to Plasma; 4d from RBC to Plasma; and 600 d from ST2 to Plasma.

Figure 10-1. Structure of the biokinetic model for systemic bismuth.

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7028

Table 10-3. Parameter values for systemic model for bismuth
To
Transfercoefficient (d-1)
PlasmaUrinary bladder contents
20
PlasmaRight colon contents
4.0
PlasmaRBC
0.5
PlasmaST0
300
PlasmaST1
4.2
PlasmaST2
1.3
PlasmaLiver 030
PlasmaKidneys (urinary path)30
PlasmaOther kidney tissue
5.0
PlasmaCortical bone surface
2.5
PlasmaTrabecular bone surface
2.5
RBC
Plasma0.173
ST0
Plasma66.54
ST1
Plasma0.0347
ST2
Plasma0.00116
Liver 0
Small intestine contents
0.208
Liver 0Liver 1
0.139
Liver 1
Plasma0.0693Kidneys (urinary path)
Urinary bladder contents
0.693
Other kidney tissue
Plasma0.139
Cortical bone surface
Plasma0.0347
Trabecular bone surface
Plasma0.0347
From

7029
7030
7031

7032
7033
7034
7035
7036
7037

(523) Model predictions are compared with the human injection data of Newton et al.
(2001) in Figures 10-1 to 10-3.

Figure 10-2. Model predictions of total-body retention of intravenously injected bismuth
compared with observations of Newton et al. (2001) for a human subject intravenously injectedwith 207Bi citrate. Retention through Day 25 estimated from excretion measurements and for
subsequent times from external measurements.

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7038
7039
7040
7041
7042

7043
7044
7045
7046
7047
7048
7049
7050
7051
7052
7053
7054
7055
7056

Figure 10-3. Model predictions of blood retention of intravenously injected bismuth comparedwith observations of Newton et al. (2001) for a human subject intravenously injected with 207Bi
citrate.

Figure 10-4. Model predictions of cumulative urinary and faecal excretion of intravenously
injected bismuth compared with observations of Newton et al. (2001) for a human subject
intravenously injected with 207Bi citrate.

10.2.3.3.

Treatment of radioactive progeny(524) The members of bismuth chains considered in the calculations of dose coefficientsfor bismuth isotopes are isotopes of lead, polonium, thallium, bismuth, or mercury. The
systemic models for these elements as progeny of bismuth isotopes are the same as theirsystemic models as progeny of lead isotopes. They are described in the section on lead.
10.3.

Individual monitoring

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7059

7060
7061
7062
7063

7064
7065
7066
7067
7068
7069
7070
7071
7072
7073
7074
7075
7076
7077
7078
7079
7080
7081
7082
7083
7084
7085
7086
7087
7088
7089
7090
7091
7092
7093
7094
7095
7096
7097
7098

210

Bi
(525) Urine bioassay is used for the monitoring of 210 Bi.
IsotopeMonitoring
Technique

210

Urine Bioassay

Bi

MethodMeasurementof Typical
DetectionLimit
1-5 Bq/L
γ-ray spectrometry

Achievabledetection limit
0.9Bq/L214

Bi(526) Whole Body counting is used for the monitoring of 214 Bi.
IsotopeMonitoring
Technique

214

Whole
Counting

Bi

MethodMeasurementof Typical
Detection
Limit
Body γ-ray spectrometry
200 BqAchievabledetection limit
36 Bq

References
Ballou, J.E., Gies, R.A., Case, A.C., Haggard, D.L., Buschbom, R.L., Ryan, J.L., 1986. Depositionand early disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat. Health Phys. 51,
755–771.
Benet, L.Z., 1991. Safety and pharmacokinetics: Colloidal bismuth subcitrate. Scand. J.
Gastroenterol. 26 (Suppl. 185), 29-35.
Boertz, J., Hartmann, L., Sulkowski, M., Hippler, J., Mosel, F., Diaz-Bone, R., Michalke, K.,
Rettenmeier, A., Hirner, A., 2009. Determination of trimethylbismuth in the human bodyafter ingestion of cooloidal bismuth subcitrate. Drug Metabolism and Disposition. 37 (2):352-358;
Boiteau, H.L., Cler, J.M., Mathe, J.F., Delobel, R., Feve, J.R., 1976. Relations entre l'evolution desencephalopathies bismuthiques et les taux de bismuth dans le sang et dans les urines. Eur. J.
Toxicol. 9, 233-239.
Buijs, W. C.; Corstens, F.H., Beentjes, L.B., 1985. ong-term retention of 207Bi in the human bodyafter injection of 206Bi. Health Phys. 49, 1267-1269.
Butterweck, G., Schuler, Ch., Vezzù, G., Müller, R., Marsh, J.W., Thrift, S., Birchall, A., 2002.
Experimental determination of the absorption rate of unattached radon progeny from
respiratory tract to blood. Radiat Prot Dosim. 102, 343–348.
Butterweck, G., Vezzù, G., Schuler, Ch., Müller, R., Marsh, J.W., Thrift, S., Birchall, A., 2001. Invivo measurement of unattached radon progeny deposited in the human respiratory tract.
Radiat. Prot. Dosim. 94, 247–250.
Coenegracht, J.M., Dorleyn, M., 1961. The distribution of intravenously administered tracer doses of
Bi-206 compounds in the human body. J. Belge de Radiologie 44, 485-504.
D’Souza, R.W., Francis, W.R., 1987. Bioavailability and pharmacokinetics of bismuth in the rat.
Pharm. Res. 4:S115 (abstract).
Dresow, B., Fisher, R., Gabbe, E., Wendel, J., Heinrich, H., 1992. Bismuth absorption from 205Bilabelled pharmaceutical bismuth compounds used in the treatment of peptic ulcer disease.
Scan. J. Gastroenterol. 27(4): 333-336.
Dresow, B., Nielsen, P., Fisher, R., Wendel, J. Gabbe, E., Heinrich, H., 1991. Bioavailibility ofbismuth from 205Bi-labelled pharmaceutical oral Bi-preparations in rats. Arch. Toxicol.
65(8), 646-650.
Drew, R.T., 1971. 212Pb distribution studies in the rat. Health. Phys. 20, 617–623.

179

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
7099
7100
7101
7102
7103
7104
7105
7106
7107
7108
7109
7110
7111
7112
7113
7114
7115
7116
7117
7118
7119
7120
7121
7122
7123
7124
7125
7126
7127
7128
7129
7130
7131
7132
7133
7134
7135
7136
7137
7138
7139
7140
7141
7142
7143
7144
7145
7146
7147
7148
7149
7150

Durbin, P.W., 1960. Metabolic characteristics within a chemical family. Health Phys. 2, 225-238.
Einhorn, J., Engstedt, L., Franzen, S., Lundell, G., 1964. Distribution of colloidal bismuth
intravenously and intraarterially administered in man. Acta Radiol. 2, 443-448.
Eridani, S., Balzarini, M., Taglioretti, D., 1964. The distribution of radiobismuth in the rat. Br. J.
Radiol. 37, 311-314.
Froomes, P.R.A., Wan, A.T., Keech, A.C., McNeil, J.J., McLean, A.J., 1989. Absorption andelimination of bismuth from oral doses of tripotassium dicitrato bismuthate. Eur. J. Clin.
Pharmacol. 37, 533-536.
Gaucher, A., Netter, P., Faure, G., 1979 Bismuth-induced osteoarthropathies. Med. J. Aust. 24:129130.
Gavey, C.J., Szeto, M.-L., Nwokolo, C.U., Sercombe, J., Pounder, R.E., 1989. Bismuth accumulates
in the body during treatment with tripotassium dicitrato bismuthate. Aliment. Pharmacol.
Therap. 3, 21-28.
Greenhalgh, J.R., James, A.C., Smith, H., 1977. Clearance of radon daughters from the lung.
NRPB/R&D1 Annual Research and Development Report 1976 pp. 49–51, Chilton, UK.
Gregus, Z., Klaassen, C.D., 1986. Disposition of metals in rats: a comparative study of fecal, urinary,and biliary excretion and tissue distribution of eighteen metals. Toxicol. Appl. Pharmacol.
85, 24-38.
Hodgson, S.A., Rance, E.R., Stradling, G.N., Hodgson, A., Fell, T.P., Youngman, M.J., Moody, J.C.,
Ansoborlo, E., 2000. Biokinetics of thorium dioxide and its decay products in the rat after
alveolar deposition: implications for human exposure. NRPB-M1192, Chilton, UK.
Hodgson, S.A., Stradling, G.N., Hodgson, A., Smith, T.J., Youngman, M.J., Moody, J.C., Ansoborlo, E.,
2003. Biokinetics and assessment of intake of thorium dioxide. Radiat. Prot. Dosim. 105, 115–
118.
Hursh, J. B., Brown, C., 1969. Tissue distribution of 212Bi in rats. Proc. Soc. Exp. Biol. Med.
131:116-120.
Hursh, J.B., Mercer, T.T., 1970. Measurement of 212Pb loss rate from human lungs. J. Appl. Physiol
28, 268–274.
Hursh, J.B., Schraub, A., Sattler, E.L., Hofmann, H.P., 1969. Fate of 212Pb inhaled by human subjects.
Health Phys. 16, 257–267.
ICRP, 1980. Limits for intakes of radionuclides by workers. ICRP Publication 30. Part 2. Oxford:
Pergamon Press.
ICRP 1975. Reference Man: Anatomical, Physiological and Metabolic characteristics. ICRP
Publication 23. Oxford, Pergamon Press.
Koch, K.M., Davis, I.M., Gooding, A.E., Yin, Y., 1996a. Pharmacokinetics of bismuth and ranitidine
following single doses of ranitidine bismuth citrate. Br. J. Clin. Pharmacol. 42, 201-205.
Koch, K.M., Kerr, B.M., Gooding, A.E., Davis, I.M., 1996b. Pharmacokinetics of bismuth andranitidine following multiple doses of ranitidine bismuth citrate. Br. J. Clin. Pharmacol.
42:207-211.
Lloyd, R.D., Mays, C.W., Taylor, G.N., Atherton, D.R., Bruenger, F.W., Jones, C.W., 1982. Radium
retention, distribution, and dosimetry in beagles. Radiat. Res. 92, 280-295.
Loiseau, P., Henry, P., Jallon, P., Legroux, M., 1976. Encephalopathies myocloniques iatrogenes aux
sels de bismuth. J. Neurol. Sci. 27, 133-143.
Marsh, J.W., Birchall, A., 1999. Determination of lung-to-blood absorption rates for lead and bismuththat are appropriate for radon progeny. Radiat. Prot. Dosim. 83, 331–337.
Matthews, C.M.E., Dempster, W.J., Kapros, C., Kountz, S., 1964. The effect of bismuth 206
irradiation on survival of skin homografts. Br. J. Radiol. 37, 306-310.
Moody, J.C., Davies, C.P., Stradling, G.N., 1994b. Biokinetics of thorium and daughter radionuclides
after deposition in the rat lung as fluoride and hydroxide. In: Mohr U., Dungworth, D.L.,
Mauderly, J.L., Oberdörster, G (Eds.), Proc. Fourth International Inhalation Symposium,
Hannover, March 1–5, 1993. Toxic and Carcinogenic Effects of Solid Particles in the
Respiratory System, pp. 611–614.

180

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
7151
7152
7153
7154
7155
7156
7157
7158
7159
7160
7161
7162
7163
7164
7165
7166
7167
7168
7169
7170
7171
7172
7173
7174
7175
7176
7177
7178
7179
7180
7181
7182
7183

Moody, J.C., Stradling, G.N., 1992. Biokinetics of thorium and daughter radionuclides after
deposition in the rat lung. J. Aerosol Sci. 23, S523–S526.
Moody, J.C., Stradling, G.N., Pearce, M.J., Gray, S.A., 1994a. Biokinetics of Thorium and Daughter
Radionuclides after Deposition in the Rat Lung as Nitrate: Implications for Human
Exposure. NRPB-M525, Chilton, UK.
Newton, D., Talbot, R.J., Priest, N.D., 2001. Human biokinetics of injected bismuth-207. Human
Exper. Toxicol. 20, 601-609.
Pieri, F., Wegmann, R., 1981. Radiopharmaceutical study of Bi-citrate in the rat. Compartmental
distribution. Cell. Molecul. Biol. 27, 57-60.
Rao, N., Feldman, S., 1990. Disposition of bismuth in the rat: I. Red blood cell and plasma protein
binding. Pharm. Res. 7, 188-191.
Russ, G. A., Bigler, R.E., Tilbury, R.S., Woodard, H.Q., Laughlin, J.S., 1975. Metabolic studies withradiobismuth. I. Retention and distribution of 206Bi in the normal rat. Radiat. Res. 63, 443454.
Slikkerveer, A., de Wolff, F.A., 1989. Pharmacokinetics and toxicity of bismuth compounds. Med.
Toxicol. Adverse Drug Exp. 4, 303-323.
Sollmann, T.A., 1957. Manual of Pharmacology and its Applications to Therapeutics and Toxicology.
Philadelphia: W.B. Saunders Co.
Sollmann, T., Seifter, J., 1942. Intravenous injections of soluble bismuth compounds: their toxicity,and their sojourn in the blood and organs. J. Pharmacol. Exp. Ther. 74, 134-154.
Stradling, G.N., Davies, C.P., Moody, J.C., Gray, S.A., Wilson, I., Ellender, M., 2005. Biokinetics ofthorium and daughter radionuclides after deposition as fluoride and hydroxide in the rat
lung: implications for occupational exposure. NRPB-DA/05/2005, Chilton, UK.
Van der Werff, J. Th., 1965. Radioactive bismuth 206Bi. Experimental studies and clinicalapplications. Acta Radiological Suppl. 243, 1-89.
Vienet, R., Bouvet, P., Istin, M., 1983. Kinetics and distribution of 206Bi in the rat and the rabbit: amodel. Int. J. Appl. Radiat. Isot. 34, 747-753.
Zidenberg-Cherr, S., Parks, N.J., Keen, C.L., 1987. Tissue and subcellular distribution of bismuth
radiotracer in the rat: considerations of cytotoxicity and microdosimetry for bismuth
radiopharmaceuticals. Radiat. Res. 111, 119-129.

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7189
7190
7191
7192
7193
7194
7195
7196
7197
7198
7199

11. POLONIUM (Z = 84)
11.1.

Chemical forms in the workplace(527) Polonium is a metalloid which mainly occurs in oxidation states IV. Bismuth andtellurium are good chemical analogues of polonium. Polonium may be encountered inindustry in a variety of chemical and physical forms, including oxides, hydroxides, acidicpolonium vapours, inorganic salts (bromides, chlorides, and iodides) and also volatile organic
forms such as dimethyl and dibenzyl-polonium. A mixture or alloy of polonium andberyllium can be used as a neutron source. Polonium is produced by the decay of 220Ra and222
Ra, which respectively belong to the 232Th and 238U natural radioactive series. The mainpolonium isotope presents in the environment is 210Po.
Table 11-1. Isotopes of polonium addressed in this report
IsotopePo-203
Po-204Po-205
Po-206
Po-207
Po-208Po-209
Po-210a

7200
7201
7202
7203
7204
7205
7206
7207
7208
7209
7210
7211
7212
7213
7214
7215
7216
7217
7218
7219
7220
7221
7222
7223

a

Physical half-life
36.7 m3.53 h
1.66 h8.8 d5.898 h2.90 y102 y138.376 d

Decay mode
EC, B+, A
EC, A
EC, B+, A
EC, A
EC, B+, A
A, EC
A, EC
A

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides are
given on accompanying electronic disk.

11.2.

Routes of Intake

11.2.1. Inhalation(528) The most important widespread exposures to radioisotopes of polonium are as decay
products of radon. The alpha-emitting isotopes 218Po (half-life 3 minutes) and 214Po (half-life
160 µs) give rise to most of the dose from inhalation of the short-lived decay products of
222
Rn, as do 216Po (half-life 0.15 s) and 212Po (half-life 310 ns) for those of 220Rn (thoron). For
the decay schemes see the uranium and thorium sections. Dose coefficients for isotopes ofpolonium inhaled as short-lived radon decay products are given in the radon section, where
factors such as the relevant aerosol size distribution are addressed.
(529) Otherwise, inhalation of 210Po (half-life 138 d) arises through its formation as thelast radioactive member of the 238U decay series, and through its use as a high specific activity
alpha-emitting source. It may be present in mineral dusts containing the whole series, or in
the atmosphere as a decay product of 222Rn via relatively long-lived 210Pb (half-life 22 years).
Workers in uranium and others mines are exposed to both. There is evidence that atmospheric210
Pb accumulates on growing tobacco leaves, leading to intakes of 210Pb and 210Po bysmokers.
(530) Applications of 210Po as a high specific activity alpha-emitter include electrostatic
charge eliminators, and neutron sources. The high specific activity gives rise to special issues,
notably the spontaneous formation of 210Po aerosol above 210Po samples. Borisov (1999)
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7224
7225
7226
7227
7228
7229
7230
7231
7232
7233
7234
7235
7236
7237
7238
7239
7240
7241
7242
7243
7244
7245
7246
7247
7248
7249
7250
7251
7252
7253
7254
7255
7256
7257
7258
7259
7260
7261
7262
7263
7264
7265
7266
7267
7268
7269
7270
7271

showed that 210Po on open surfaces releases particles ranging from individual 210Po atoms toaggregates of >3000 atoms. Borisov (1999) also reported that gaseous polonium is present inaerosols containing 210Po, resulting in some penetration of fibrous filters, and that the gaseous
fraction formed in moist air resembles polonium hydride (PoH2), which is unstable,
decomposing to polonium and hydrogen.
Absorption types and parameter values(531) Information is available on the behaviour of polonium following deposition in the
respiratory tract from animal experiments with several chemical forms, and from some
accidental human intakes.
(532) However, the behaviour of ionic (soluble) Po following deposition in the respiratory
tract is difficult to determine because ionic solutions (e.g. chloride) are unstable at neutral pH
and in many biological media, resulting in colloid formation. Adsorption of polonium onto
surfaces has caused experimental problems, e.g. in determining amounts administered. All theexperiments described below used 210Po, because of its relatively long half-life andavailability, but as its yield of penetrating photons is very low, direct external counting could
not be used to estimate initial deposits or whole body content in vivo. Analysis ofexperimental data to derive absorption parameter values is difficult. Excretion of systemicpolonium is mainly fecal, and so fecal excretion does not enable particle transport from therespiratory tract to be easily distinguished from absorption. There is also significant
absorption of polonium in the alimentary tract (~10%), and in inhalation experiments, withhigh deposition in the extrathoracic airways and rapid clearance to the alimentary tract, thiscontributed to early uptake to blood, along with the rapid phase of absorption from therespiratory tract. Studies of polonium hydroxide colloid administered to rats by intratracheal
instillation and nose-only inhalation are considered first, because they provide the mostdetailed information on the rapid phase of absorption. In deriving absorption parametervalues from the results of studies using rats, the systemic model structure described in section
3 below was used, but it was modified using information from the polonium hydroxide
studies (Thomas and Stannard 1964; Casarett 1964) and from intravenous injection
experiments in rats conducted at the same institute (Stannard 1964).
(533) Absorption parameter values and Types, and associated fA values for particulate
forms of polonium are given in Table 11-2.
Polonium hydroxide colloid (PoO(OH)2)(534) Thomas and Stannard (1964) studied the tissue distribution and excretion of 210Po
after intratracheal administration into rats of a freshly neutralised solution of 210Po in 0.5N
HCl. This preparation was termed "polonium hydroxide colloid" by Morrow and Della Rosa
(1964), referring to Morrow et al. (1964) who investigated the formation of polonium
colloids. According to Morrow and Della Rosa (1964) it consists almost entirely of colloid
particles less than 50 Å (5 nm) in diameter. One group of 30 rats was used to study the shortterm biokinetics, with emphasis on lung clearance: seven were sacrificed during the first 24
hours, and the rest at times up to 62 d (further details are given in Thomas and Stannard
1956). Another 39 were used for a long-term experiment with measurements up to 478 d.
Lung retention at 1, 10 and 60 d after administration was estimated to be ~70%, 45% and 5%of the initial lung deposit (ILD) (after correction for incomplete recovery in 210Po
measurements, and blood-borne 210Po). The distribution of systemic activity was broadly
similar to that observed following intravenous injection into rats of a similar 210Po preparation(Stannard 1964). The fecal to urine excretion ratio was >20 during the first week, during
183

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which about 4% ILD was excreted in faeces, presumably reflecting particle transport from thebronchial tree to the alimentary tract. After 10 days the ratio was ~10, similar to that observed
after intravenous injection (Stannard 1964), indicating that most of the excretion was
systemic. Analysis carried out here (i.e. by the Task Group) of the results of the short-term(62-d) study, assuming that the 210Po retained in the lungs was in particulate form rather thanbound (fb = 0, see below) gave absorption parameter values of fr = 0.5; sr = 2 d–1 and ss = 0.02
d–1. Analysis of the results of the long-term study gave similar values of fr and sr, but a lower
value of ss, ~0.01 d–1. (Both sets of parameter values give assignment to Type M.)(535) Casarett (1964) followed the distribution and excretion of 210Po following brief (20minute) nose-only exposure of 44 rats to polonium hydroxide colloid (neutralised 210Po
chloride) carried on a sodium chloride vector aerosol (count median diameter, CMD, 0.05µm). Further details are given by Casarett (1958). Six rats were sacrificed immediately after
exposure, the rest in pairs at times up to 30 d, including nine time points in the first 24 hours,
giving unusually detailed information on the rapid phase of respiratory tract clearance for an
inhalation experiment. Complete urine and fecal collections were made for each rat, which
also enabled the "dose", i.e. the initial total deposit (ITD) in each rat to be estimated. The
measurements of activity distribution were complemented by a comprehensive
autoradiographic study. The amounts of 210Po in the alimentary tract and faeces in the first
three days indicate that about 60% ITD was deposited in the upper respiratory tract (URT, theskinned head and trachea) and bronchial tree. (However, this might also have included someingestion of 210Po deposited on the pelt during preening.) The particle clearance rate to thealimentary tract was estimated here to be about 10-15 d-1 (half-time of 1.5 hours). The
assumption that this clearance was predominantly by particle transport sets an upper limit of~10 d–1 on the rapid absorption rate (sr). Casarett (1964, p. 158) reported that "Duringexposure, about 20% of the deposited load left the lung and was translocated to othertissues..." which would imply a value of sr of the order of 100 d–1. The basis for thisinference is not apparent from the tissue or blood data presented in that paper, but Casarett(1958 pp. 151-152) relates it to the presence of ~25% ITD in the "residual carcass", in thefirst few measurements (which fell to ~4% ITD by 1 d, and remained at that level thereafter).
However, it appears that this might well have included most if not all of the pelt, and it isplausible that the transient high 210Po content could have been due to external contamination.
Since it seems inconsistent with amounts in blood and other tissues, it was not included inanalyses carried out here. Similarly, Casarett (1964) noted that the appearance of highexcretion (~4% ITD) in urine in the first 12 hours was evidence for rapid absorption.
However, whereas the urinary excretion rate was much higher during the first few days (> 1%
ITD d–1) than subsequently (typically < 0.1% ITD d–1), this was not observed after
intratracheal instillation of similar material (Thomas and Stannard 1964), for which the ratewas ~0.07% d–1 during the first week. It seems plausible that the high early excretion rate
after inhalation was due to contamination from the pelt, as noted by Kimball and Fink (1950).
Bailey et al. (1985) similarly observed much higher urinary excretion of 85Sr by rats in thefirst few days after nose-only inhalation than after instillation of 85Sr-labelled fusedaluminosilicate particles, and that most of the activity in such samples was removed byfiltration, and was therefore probably particulate contamination. The early urine data were
not therefore included in analyses here. Lung retention at 10 and 30 days after exposure was~37% and 17% of the lung content at the end of exposure. As for the instillation experiment,
the fecal to urine excretion ratio after 10 days was ~10, similar to that observed after
intravenous injection (Stannard 1964), indicating that most of the excretion was systemic.
(536) The content of the upper respiratory tract (URT, based on the skinned head and184

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trachea) fell rapidly from ~30% ITD immediately after exposure, to ~2% ITD at 8 – 24 hours.
Casarett (1958 p. 166) alluded to retention of ~2% ITD in the trachea throughout the 30-dstudy period. He considered it more likely to represent 210Po in associated structures (e.g.
lymphatic tissues) than 210Po in transit from lungs to alimentary tract. This could be evidenceof a bound fraction, but could include contributions from other sources, such as systemic210
Po (see below). Autoradiographs of the lungs throughout the 30 d showed both clusters ofalpha tracks, and many individual tracks, indicating the presence of both particulate and ionic210
Po. Casarett (1958 p. 97) judged that most of the 210Po in the lungs appeared to be inparticulate form.
(537) Analysis carried out here, assuming that the 210Po retained in the lungs was inparticulate form rather than bound (fb = 0, see below) gave absorption parameter values of fr =0.1; sr = 2 d–1 and ss = 0.03 d–1, giving assignment to Type M. The values of sr and ss are ingood agreement with those derived above for the short-term instillation experiment. The
value of fr is lower, which might reflect a difference resulting from the method ofadministration, or a higher proportion of colloidal material in the inhalation experiment. The
value of sr (rounded to 2 d–1) was therefore used in the analyses of results of otherexperiments with similar forms of polonium, but for which there were insufficient data todefine sr.
(538) Smith et al. (1961) determined the distribution of 210Po at approximately 1, 4 and 5
months after inhalation by six dogs of polonium hydroxide colloid (neutralised 210Po
chloride) carried on a sodium chloride vector aerosol (CMD, 0.04 µm), similar to that inhaledby rats (Casarett 1964). Urine and fecal excretion were also measured. Further details(including daily excretion and additional tissue measurements) are given by Smith et al.
(1960). However, there are differences in some of the results reported in the two documents.
(Some, but not all, could be attributed to decay correction being made in the 1961 paper but
not in the 1960 report.) Since the 1961 paper refers to the other as an earlier version, it wasused as the definitive source in analyses carried out here. About 50% of the ITD cleared in~3 d, which was attributed to clearance from the URT, suggesting that the rapid dissolution
rate is slow compared to particle transport from the URT. The other ~50% of 210Po in the
body was retained with a half-time of 37 d. Lung retention after 30 days as a fraction of theremaining body content decreased with a half-time of 36 d. Since particle transport from thelungs of dogs is so slow, this would have been mainly by absorption. Analysis carried out
here gave values of fr ~0.3 and ss = 0.03 d–1, assuming that the 210Po retained in the lungs wasin particulate form rather than bound (fb = 0, see below); and that sr = 2 d–1 (based on the
more detailed studies with polonium hydroxide in rats, see above). These are in broad
agreement with the studies in rats described above, and also give assignment to Type M.
Autoradiography of tissues from dogs sacrificed at 28 and 29 d showed uniform distributionof 210Po as single tracks, except for lesser concentrations in and on tissues of the bronchialtree. (This might suggest lung retention in the bound state rather than particulate form, see
below.)(539) Morrow and Della Rosa (1964) studied the tissue distribution and excretion of 210Po
after intratracheal administration to seven rabbits of a freshly neutralised stock solution of210
Po in 0.5N HCl. Further details are given by Morrow and Della Rosa (1956). For two
rabbits the neutralised solution was aged for a week in order to increase the fraction ofpolonium colloid, but no differences in retention characteristics were noted between the two
preparations, and the results were combined. At 2 d after administration the lungs contained
about 60% ILD. The authors estimated that of the 40% cleared about half was in thealimentary tract and contents and half (i.e. ~20% ILD) absorbed into blood, indicating a value
185

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7380
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7382
7383
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7386
7387
7388
7389
7390
7391
7392
7393
7394
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7396
7397
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of fr ~0.2. Since the first measurement was at 1 day, only a lower limit on sr can be set of ≥ 1
d–1. At 10 and 30 d the lungs contained about 24% and 2% ILD, respectively. These values
are significantly lower than those obtained in the experiments with rats (45% and 18%
respectively, Thomas and Stannard, 1964). From 2 to 30 d lung retention could be represented
by a single exponential function with a rate of 0.12 d–1 (half-time ~5.7 d). This is an upper
limit on ss, because some of the clearance was due to particle transport. However, the rate ofparticle transport from the rabbit lung is not known. (Rabbits have not often been used to
study alveolar clearance.) The authors estimated that ~60% ILD had been absorbed from thelung by 30 d, which suggests that absorption was the dominant clearance process and hence
that ss is likely to be in the range 0.05 - 0.1 d–1. This is much faster than assessed for rats or
dogs, and would give assignment to Type F. Another inter-species difference, compared torats, is the much higher urinary excretion in rabbits than in rats, the ratio of faecal to urine
excretion being about 0.5 after 10 d. Higher urinary excretion in rabbits than in rats was also
observed after intravenous injection (Silberstein et al., 1950a). In four other rabbits the 210Po
was attached to silver particles (<10 µm diameter) before neutralisation (only reported inMorrow and Della Rosa, 1956). The biokinetics of 210Po were broadly similar to thosefollowing administration of hydroxide colloid alone. Lung clearance was even faster:retention could be represented by a single exponential function with a rate of 0.25 d–1 (halftime ~2.8 d). Surprisingly, this did not appear to result from greater particle transport to thealimentary tract, but to greater absorption: whole body retention and urinary excretion werehigher, and fecal excretion was lower. Complementary autoradiographic studies (on the samerabbits, with or without silver particles) were reported by Casarett (1958). It was noted thatmost of the activity was usually found in one lung lobe. As in the rat studies, autoradiographsof the lungs throughout the 28 d showed both clusters of alpha tracks, and many individual
tracks, indicating the presence of both particulate and ionic 210Po.
(540) Although specific parameter values for polonium hydroxide based on in vivo data are
available, they are not adopted here, because inhalation exposure to it is unlikely, and because
they are similar to those for default Type M. Instead, polonium hydroxide is assigned to TypeM.
Polonium chloride (PoCl2; PoCl4)(541) Berke and DiPasqua (1964) followed the biokinetics of 210Po in rats for 60 d after a
5-hour whole-body exposure to 210Po chloride carried on a sodium chloride vector aerosol(CMD 0.1 µm). However, whereas the aerosols administered in the studies described in thesection on polonium hydroxide colloid were neutralised, in this experiment the solution wasacidified (0.1N HCl). This might have resulted in a greater proportion of the 210Po being inionic, rather than colloidal form. Further details are given by Berke and DiPasqua (1957).
With a relatively long exposure and few early measurements (immediately after exposure, 1
and 3 d) there is little information to define sr. The whole body exposure resulted in extensive
contamination of the pelt, which would have affected early excretion measurements. Preening
would have led to ingestion of an indeterminate amount of 210Po, and absorption from thealimentary tract to blood, making it difficult to estimate early uptake from the respiratory
tract. Lung retention of 210Po at 10, 30 and 60 d was about 44%, 15% and 10% of the ILD(based on the estimated lung content at the end of exposure). These results are similar to
those observed following administration of polonium hydroxide (Casarett 1964, Thomas andStannard 1964, see above). Activity in the URT (skinned head) was about 12% of the bodycontent (excluding pelt and alimentary tract) immediately after exposure. This fell rapidly toabout 3% of the body content, and remained at that level throughout the experiment. Berke186

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and DiPasqua (1957) suggested that this might be due to continuing ingestion e.g. of excreta.
Analyses carried out here gave absorption parameter values of fr = 0.4 and ss = 0.01 d–1,
assuming that the 210Po retained in the lungs was in particulate form rather than bound (fb = 0,
see below); and that sr = 2 d–1 (based on the more detailed studies with polonium hydroxide,
see above). These parameter values give assignment to Type M. The value of ss is broadly
similar to values derived from studies using polonium hydroxide (see above). A central valueof 0.015 d–1 was therefore used in the analyses of results of other experiments with similar
forms of polonium, but for which there were insufficient data to define ss.
(542) Although specific parameter values for polonium chloride based on in vivo data are
available, they are not adopted here, because inhalation exposure to it is unlikely, and because
they are similar to those for default Type M. Instead, polonium chloride is assigned to TypeM.
Volatilised polonium (oxide)(543) Kimball and Fink (1950) investigated the biokinetics of 210Po for 10 d after a brief
inhalation of volatilised polonium by rats. The aerosol was produced by deposition of 210Po
from solution onto a nickel foil, through which a current was passed until it was red hot. The
chemical form was not investigated, but oxide is mentioned in the report. Measurements ofthe diffusion coefficient of Po ions newly formed by decay of radon indicate that they exist ina variety of chemical forms as a result of interaction with components of air (see e.g. Busigin
et al., 1981). According to Chu and Hopke (1988), Po ions are rapidly converted to PoO2+ inthe presence of oxygen. In one experiment (individual nose-only inhalation for 10–60 s), lungretention fell to ~60% ILD at 24 hours, and ~10% ILD at 10 d. The authors assessed that lungclearance was mainly by absorption to blood. Although data were not given, it was stated that(when extreme precautions were taken) animals sacrificed within a few minutes of exposure
showed only traces of activity outside the respiratory tract, suggesting that the rapid
absorption was on a time-scale of hours rather than minutes. In another experiment, (group of
20 rats, simultaneous head-only 15-minute inhalation) lung clearance appeared to be slower,
falling from ~40% ILD at 24 hours to ~30% ILD at 10 d. Analyses carried out here gave
values of fr ~0.4 for both experiments, assuming that the 210Po retained in the lungs was inparticulate form rather than bound (fb = 0, see below); and that sr = 2 d–1 and ss = 0.015 d–1(based on more detailed studies with polonium hydroxide, see above). These parametervalues give assignment to Type M. Retention of material in the URT (based on the skinned
head and trachea) was reported, of the order of 10% of the estimated initial deposit in the
URT. This could be evidence of a bound fraction, but could include contributions from othersources, such as systemic 210Po (see below). Autoradiography of lungs from a rat sacrificed
immediately after inhalation showed uniform distribution of 210Po in alveolar tissue and clear
deposition throughout bronchi and bronchioles. However, the authors noted that by 24 hours
after inhalation autoradiography showed only a little remaining in the bronchial walls.
(544) Although specific parameter values for volatilised polonium based on in vivo data
are available, they are not adopted here, because of the uncertainty on them, and because they
are similar to those for default Type M. Instead, volatilised polonium is assigned to Type M.
Mineral dusts(545) Intakes of 210Po in particulate aerosol form can arise from exposure to airborne
mineral dusts containing the natural long-lived parent 210Pb. In this case the absorption rate
will probably be determined by the dissolution rate of the mineral matrix in lung fluids.
Measurements have been made of the dissolution in simulated lung fluid of samples of coal187

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fly ash (Kalkwarf et al., 1984) and condensate from calcining phospate rock dust (Kalkwarf
and Jackson 1984) for 60 days. By this time the amounts of 210Po dissolved were <0.2% and<1% respectively, indicating assignment to Type S in both cases.
Polonium condensed with cigarette smoke tar(546) Although mainly related to environmental, rather than occupational, exposure
information relating to 210Po in tobacco smoke is included here for completeness. Polonium210 and its precursor, 210Pb, are inhaled in cigarette smoke (Holtzman 1967; Little andRadford 1967; Parfenov 1974; Cross 1984; Skwarzec et al., 2001; Desideri et al., 2007).
Higher concentrations of 210Po have been measured in the lungs of smokers than in nonsmokers, indicating that not all the 210Pb and 210Po inhaled are readily soluble (Little et al.,
1965; Rajewsky and Stahlhofen 1966; Holtzman and Ilcewicz 1966). It has been reported that210
Pb is concentrated in resinous material in the tips of trichomes (hairs) on the surfaces oftobacco leaves, which forms relatively insoluble particles during combustion (Martell 1974;
Radford and Martell, 1975). The 210Po present probably vaporises during combustion, but
grows in from decay of 210Pb after deposition in the respiratory tract.
(547) Cohen et al., (1979) measured the concentration of 210Po in the tracheobronchial tree
(TB) and parenchyma (alveolar interstitial, AI region) of tissues obtained at autopsy fromsmokers, ex-smokers, and non-smokers. In non-smokers, the ratio of 210Po concentration in
TB to that in AI was ~3 (resulting mainly from systemic 210Pb/210Po). In smokers and exsmokers, the ratio was ~1: the higher concentration of 210Po in the parenchyma was attributed
to the retention of relatively insoluble particles containing 210Pb/210Po inhaled in cigarettesmoke. Cohen et al. (1980) measured the dissolution (in physiological saline at 37°C) of
alpha-activity of cigarette smoke collected on membrane filters. No decrease in activity wasobserved (estimated upper limit on dissolution ~20%), although there was a considerable
reduction in sample mass. Cohen et al. (1985) measured 210Po in the lungs of rats at times
during exposure for 6 months to smoke from cigarettes enriched in 210Pb/210Po, and up to 5
months afterwards. A two-component compartment model was fit to measurements of lungretention following the end of exposure: a good fit was obtained with 90% cleared at a rate of
0.036 d–1 (half-time 19 d) and 10% was cleared at a rate of 0.0055 d–1 (half-time 125 d). This
indicates Type M or S behaviour for both the 210Pb and the 210Po.
Unknown form (accidental exposures of workers)(548) Follow-up data for many cases of apparently acute inhalation of 210Po by workers
have been reported, but in a high proportion only urine (and in some cases blood)measurements were reported, and in such cases little can be inferred about respiratory tract
absorption (see e.g. Naimark 1948, 1949, and section 3 below). Some cases are considered
here: in most of these, urine and fecal excretion measurements were reported. The biokinetic
models used in this document predict that for inhalation of a 5-µm AMAD aerosol by areference worker, the ratio of daily fecal excretion to daily urinary excretion (F/U) is fairly
constant from about 10 d after intake, being ~3 for default Type F or Type M 210Po (which
does not allow a distinction to be made between them), and ~40 for Type S. However, in theirreview, Leggett and Eckerman (2001) pointed out that a technique widely used for routine
workplace monitoring of 210Po in urine involved spontaneous deposition of 210Po onto a metal
disc, without prior acid digestion, and this could underestimate the activity present. In none of
the cases considered in this section was it reported that acid digestion was used prior to 210Po
deposition onto a metal disc, and so any conclusions must be treated with caution, since theurine measurements may have been underestimated, and the ratio F/U overestimated.
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(549) Foreman et al. (1958) reported excretion data for two physicists who were exposed
to 210Po for at most a few minutes after the rupture of a Po-Be source, for ~200 d after theincident (urinary excretion for both, and faecal excretion for one). Both urinary and faecal
excretion showed at least two phases. The estimated biological half-time of the first (rapid)
urinary component, representing about 6% of total urinary excretion, was 0.75 d. The ratio
F/U was approximately 20 over the period 10–100 d, suggesting behaviour between Types M
and S. Analysis here, using the systemic model described in section 3, and the updated
HRTM (inhalation of a 5-µm AMAD aerosol by a reference worker) with sr = 2 d–1, gave
estimated parameter values fr = 0.02 d–1, ss = 0.001 d–1.
(550) Sheehan (1964) analyzed blood, urine, and faeces of a worker who inhaled 210Po inacid vapours. Measurements apparently started several days after exposure. Urine and blood
both showed a biological half-time of 43 d. Total urinary and faecal excretion determined fordays 47-52 post exposure indicated a ratio F/U of 6.5, suggesting behaviour between Types M
and S, but closer to Type M.
(551) Scott and West (1975) measured excretion of 210Po in urine and faeces for 160 d,starting an estimated 2 days after the presumed accidental inhalation by a worker of material
from a 210Po source. Contamination was found throughout the room. Although the paper's
summary refers to "an exposure to 210-Po oxide...", the only information on chemical form
given is that the source was made by vapour-depositing polonium metal onto a metal disc.
Only ~3% of the estimated activity deposited in the respiratory tract was excreted in the urine.
(The urine data showed very high day-to-day variation.) The ratio F/U was in the range 20-30
over the period 10 - 110 d, suggesting behaviour between Types M and S.
(552) Ilyin (2001) reported measurements on a worker who died as a result of a large
accidental intake of 210Po by inhalation (no information was given on its form). Reported
activities retained at death, 13 days after intake, were: whole body 100 MBq, lungs 13 MBq,
kidney 4.5 MBq and liver 21 MBq. The daily excretion rate was reported to be 1.6 MBq d–1(urine 25.5%, faeces 33.8%, vomit 32.4%, saliva 7.1% and sweat 1.2%). Harrison et al.
(2007) discussed the reported symptoms in relation to estimated tissue doses. They obtained aconsistent fit to the urine and post-mortem tissue measurements using the Publication 66
Type M default values of sr (100 d–1) and ss (0.005 d–1) but with higher values of fr andfractional intestinal absorption than the default values. Analysis here, using the systemic
model described in section 3, and the updated HRTM (inhalation of a 5-µm AMAD aerosol
by a reference worker) with sr = 2 d–1, ss = 0.005 d–1, and fA constrained to 0.1*fr (see Table
11-2, footnote c), gave a consistent fit to post-mortem tissue measurements with fr ~0.7. The
result was insensitive to the choice of sr. The F/U ratio was lower (~1.3) than predicted by
the systemic model used here, but may have been affected by the response to the radiation,
which included severe vomiting.
Default rapid dissolution rate for polonium(553) Studies with polonium hydroxide colloid give values of sr of about 2 d–1. This is
close to the general default value of 3 d–1 for Type M and S materials, and in view of theuncertainties in assessing absorption parameter values for polonium, a value of 3 d–1 is also
applied here to all Type F forms of polonium.
Extent of binding of polonium to the respiratory tract(554) The studies with polonium hydroxide, chloride, and volatilised polonium (oxide) all
suggest that there is respiratory tract retention of polonium deposited in ionic (soluble) form.
However, whether this is retained in particulate or bound form is unclear. Because of colloid
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formation at and around neutral pH, some colloid formation before deposition in the
respiratory tract almost certainly occurred with polonium hydroxide, and may have occurredwith the other materials. Similarly colloid formation may well have occurred after deposition.
Thus formation of some particulate material would be expected.
(555) The high proportion of systemic excretion going to faeces makes it difficult todistinguish clearance by absorption from clearance by particle transport and hence the extent
of any bound fraction. As noted above, in several studies, retention of 210Po in the upper
respiratory tract (URT) was noted, and might be considered to be evidence of a boundfraction. However, this was usually based on retention in the skinned head, which would haveincluded 210Po in soft tissues, blood and lymphatics. Clearance from the URT appeared to be
slower than from the lungs: if retention in the respiratory tract were due predominantly to abound fraction, then the rate of uptake to blood should be similar from the URT and lungs.
Autoradiographic studies which complemented the radiochemical measurements of activity
distribution and excretion also indicated the presence of both particulate and ionic 210Po. The
latter might be considered to be evidence of a bound fraction, but some would have beensystemic or blood-borne. Another indication of retention in a bound, rather than particulate
form, is the similarity in the retention kinetics of different chemical forms administered,suggesting the retention is characteristic of the element rather than related to dissolution ofdifferent particulate forms (see lead section). Thus there are indications that there might well
be some binding of polonium. However, the information is insufficient to estimate the extent
of the bound state with confidence. Although it is not clear that the bound state for polonium
is negligible, it is assumed by default that fb = 0.
Table 11-2. Absorption parameter values for inhaled and ingested polonium
Absorption
parameter Absorption fromavaluesthealimentaryfrsr (d–1) ss (d–1) tract, fA

Inhaled particulate materials
Default parameter valuesb,cAbsorption
Assigned forms
Type
F
—
1
M
Chloride,hydroxide, 0.2
volatilisedpolonium,allunspecified formsd
S—
0.01
Ingested material
All chemical forms
7585
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7591
7592
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7595

3
3

–
0.005

0.1
0.02

3

1x10–4

0.001

0.1

a

It is assumed that for polonium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F
forms of polonium (3 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default
values.
b
Materials (e.g. polonium chloride) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see text).
c
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the product of fr for the absorption
Type and the fA value for ingested soluble forms of polonium (0.1).
dDefault Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

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7597
7598
7599
7600
7601
7602
7603
7604
7605
7606
7607
7608
7609
7610
7611
7612
7613
7614
7615
7616
7617
7618
7619
7620
7621
7622
7623
7624
7625
7626
7627
7628
7629
7630
7631
7632
7633
7634
7635
7636
7637
7638
7639
7640
7641
7642
7643

11.2.2. Ingestion(556) Fractional absorption of 210Po from the alimentary tract has been measured in humansubjects and in animals (see review in Harrison et al., 2007; Scott, 2007).
(557) A male patient being treated for chronic myeloid leukaemia was reported to be
volunteer for ingestion of 7Bq/Kg body mass in drinking water. Blood concentrations andurinary excretion after administration were about one-tenth of corresponding values obtainedin other subjects after intravenous injection of polonium chloride, suggesting an f1 of0.1(Silberstein et al., 1950b;Fink 1950). Leggett and Eckerman (2001) reanalysed these dataand estimated that absorption was at least 0.15.
(558) The absorption of 210Po in animals has been reported for rats, guinea pigs and cats. In
rats, the fractional absorption has been reported as 0.03-0.06 for an unspecified chemical
form (Anthony et al., 1956) and 0.06 for the chloride (Della Rosa et al., 1955). In a study of
two rats exposed by gavage to approximately 20MBq/Kg body mass of freshly neutralized
210
Po-chloride, fractional absorption was estimated as 0.024 and 0.048 (Cohen et al., 1989).
Haines et al. (1993) obtained values for rats of 0.05 for the nitrate forms. For 210Po
administered as the citrate, absorption was reported as 0.07 - 0.09 in rats and guinea pigs.
After administration by gavage of 0.52 Mbq /Kg body mass to rats (chemical form notspecified) the f1 was found to be 0.03-0.05 (Spoerl and Anthony 1956).
(559) Fractional absorption in animals seems to be identical in males and females.
Stannard (1964) reported average f1 values of 0.05 for male rats and 0.045 for female rats
based on balanced studied after correcting for the amount of Po assumed to be excreted into
the intestine via the bile (see review in Scott 2007).
(560) In a series of experiments by Morrow et al., (1964) cats were administered by gavage
either a colloidal hydroxide or soluble citrate form of 210Po. After placing 210Po in thestomach, 0.6 to 1.6% were absorbed, independent of chemical form over a 7h-period.
However, significant differences were found for the two isotopes when the solution wasplaced in isolated duodenal loops of the small intestine. During a 10h-period, absorption was
up to 40 times greater for the citrate solution. The authors indicated that in the stomach,gastric acidity converted the colloidal 210Po to a soluble form, making absorption comparable
to the monomeric citrate form.
(561) In Publication 30 (ICRP, 1979), an f1 value of 0.1 was recommended. A higher valueof 0.5 applied to Po in foodstuff (ICRP 1993). In this report, an fA value of 0.1 is used for all
chemical forms in the workplace.
11.2.3.

Systemic Distribution, Retention and Excretion

11.2.3.1. Summary of the database
Human subjects - occupational data
(562) Leggett and Eckerman (2001) reviewed records of about 1500 former polonium
workers and estimated urinary half-times for numerous cases of apparently elevated, acuteexposure. Approximately 95% of the derived effective half-times were in the range 8-52 d,corresponding to a range of biological half-times of 8.5-83 d. The mean, median, and modeof the effective half-times were approximately 30 d, 30 d, and 34 d, corresponding tobiological half-times of 38 d, 38 d, and 45 d, respectively.
(563) Silverman (1944) reported data for a male worker who was exposed while handling a
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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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7645
7646
7647
7648
7649
7650
7651
7652
7653
7654
7655
7656
7657
7658
7659
7660
7661
7662
7663
7664
7665
7666
7667
7668
7669
7670
7671
7672
7673
7674
7675
7676
7677
7678
7679
7680
7681
7682
7683
7684
7685
7686
7687
7688
7689
7690
7691

foil containing 44.4 GBq of 210Po. Daily urine sampling and weekly fecal sampling began
immediately and continued for 64 d. Biological half-times of 34.9 d and 29.3 d were derived
from urinary and fecal excretion data, respectively.
(564) Sheehan (1964) described a case in which a worker punctured his finger with a wire
contaminated with 210Po. Daily urinary excretion of 210Po decreased by about a factor of 4
during the first 2-3 d after the incident and then decreased with a biological half-time of about
29 d over the next 14 wk.
(565) Testa (1972) described a case in which a 59-y-old woman contaminated her hands bycleaning a chemical hood where a 210Po nitrate solution had been handled. Both ingestion
intake (from a habit of finger sucking) and absorption through the skin were suspected.
Urinary excretion measurements were initiated about one week after the incident. These data
indicated a biological half-time of 29 d, but an early, rapid component may have been missed
since the first measurement was at day 7 or 8, and the urinary excretion rate fell by more thana factor of 2 between the first measurement and the second, which was made about 10 d later.
(566) A solution containing 210Po was accidentally splashed on the face of a female
technician at Mound (Cohen et al., 1989). Measurements of 210Po in urine, faeces, and bloodover several months indicate biological half-times of 13.1 d, 28.6 d, and 20.3 d, respectively.
(567) Wraight and Strong (1989) described a case in which a worker was exposed to 210Po
through a puncture wound of the thumb. The authors derived biological half-times of 35 d,
40 d, and 26 d from measurements of 210Po in urine, faeces, and blood, respectively. Fecal
excretion of 210Po was highly variable, and only one fecal measurement was made at times
greater than about 1 mo after the incident. Urinary data for this subject may be more
precisely described in terms of two excretion phases with biological half-times of about 5 d(representing about 30% of total urinary excretion) and 42 d (Leggett and Eckerman, 2001).
(568) Follow-up data for several cases of apparently acute inhalation of 210Po by workers
have been reported (e.g. see Naimark 1948, 1949; Spoerl 1951; Jackson and Dolphin 1966).
Estimated biological half-times for individual subjects, based for the most part on urinary
excretion data, generally fall in the range 20-60 d. Central estimates for relatively large
groups of workers usually are in the range 30-50 d. These half-times reflect combined
retention times in the respiratory tract and systemic tissues. Selected incidents are described
below.
(569) Foreman et al. (1958) reported urinary and fecal excretion data for two physicists
who were exposed to airborne 210Po for at most a few minutes after the rupture of a Po-Be
source. Both urinary and fecal excretion showed at least two phases. The estimatedbiological half-time of the first (rapid) urinary component, representing about 6% of total
urinary excretion, was 0.75 d. The estimated biological half-time of the first fecalcomponent, representing roughly 60% of total fecal excretion, was about 0.6 d. Urinary as
well as fecal data for times greater than a few days after exposure indicate a biological halftime of about 40 d, based on reevaluation of the plotted data (Leggett and Eckerman, 2001).
(570) Sheehan (1964) analyzed blood, urine, and faeces of a worker who inhaled 210Po inacid vapors. Measurements apparently started several days after exposure. Urine and blood
both showed a biological half-time of 43 d. Total urinary and fecal excretion determined fordays 47-52 post exposure indicated a faeces to urine ratio of 6.5. The technique used tomeasure 210Po in urine did not involve wet-ashing of samples and thus could haveunderestimated urinary excretion of 210Po (Fellman et al., 1989).
(571) Scott and West (1975) measured excretion of 210Po in urine and faeces of a worker
following accidental inhalation of material thought to consist of small particles of 210Po
oxide. Urine sampling began about 2 d after the exposure, and fecal sampling began 2 d later.
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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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7693
7694
7695
7696
7697
7698
7699
7700
7701
7702
7703
7704
7705
7706
7707
7708
7709
7710
7711
7712
7713
7714
7715
7716
7717
7718
7719
7720
7721
7722
7723
7724
7725
7726
7727
7728
7729
7730
7731
7732
7733
7734
7735
7736
7737
7738
7739

A biological half-time of 33 d was estimated from the urinary excretion data, but the data arehighly variable and not closely represented by a single half-time.
Human subjects - controlled studies(572) Silberstein et al. (1950b) measured 210Po in the urine, faeces, and blood of fourvolunteers (Subjects 1-4) who were administered 210Po chloride by intravenous injection andin a fifth volunteer (Subject 5) who ingested 210Po chloride. Subject 1 was suffering fromgeneralized lymphosarcoma, Subject 2 from acute lymphatic leukemia, and Subjects 3-5 fromchronic myeloid leukemia. Observations on Subjects 1, 2, 3, 4, and 5 were continued for up
to 43, 6, 71, 13, and 228 d, respectively. Biological half-times fitted to the time-dependent
concentration of 210Po in urine, faeces, or blood of these subjects varied somewhat with theobservation period and also showed considerable intersubject variability. For the subjects
who were followed for several weeks or months (Subjects 1, 3, and 5), urinary excretion data
indicate half-times of 30-50 d for the period starting 1 wk after exposure; fecal excretion data
indicate half-times of 33-52 d for this period; and data for red blood cells indicate half-timesof 12-48 d for this period. Urinary excretion data for the first week after administration yieldbiological half-times as short as 3 d.
(573) Excretion data for the subject of Silberstein et al. who ingested 210Po chloride(Subject 5) were reanalyzed in an attempt to determine fractional absorption from the GI tract.
Under the assumption that all fecal excretion at times greater than one week after ingestion
was due to secretion of systemic 210Po into the GI tract, it is estimated that endogenous fecal
excretion represented at least 14% of ingested 210Po. Measurements of urinary excretionindicate that approximately 0.5% of the ingested amount was removed in urine. Thus, itappears that at least 14.5% of the ingested amount was absorbed to blood. The estimate of
0.5% for urinary excretion may be an underestimate due to problems with the measurement
technique (Fellman et al., 1989).
(574) Subject 2 of Silberstein et al. died of acute lymphatic leukemia six days after
injection of 210Po. The distribution of 210Po was determined from tissue samples taken about
one hour after his death. The usefulness of the data for this subject are limited not only by thefact that he was terminally ill but also because estimated recovery of polonium wassubstantially greater than 100%, probably due to substantial overestimates of the mass ofsome tissues. For example, skin was estimated to represent 18% of body weight, which isabout fourfold greater than the relative mass of skin given in the ICRP’s Reference Man
document (ICRP, 1975). For purposes of the present study, the distribution of polonium inthe human subject has been recalculated on the basis of current information on typical organ
weights and by constraining organ contents to achieve mass balance.
(575) Hunt and Allington (1993) determined urinary 210Po in six subjects who had ingested
crab meat containing elevated concentrations of this radionuclide. Urinary excretion rates
were determined for periods of 9-21 d in five of the subjects. Biological half-times of 3-8 d
are indicated by these short-term data. Comparison of fecal excretion data with the ingested
amounts indicates that fractional absorption to blood ranged from about 0.6 to more than 0.9
in the six subjects. Urinary excretion over the first 7 d represented 0.4-1.1% of the absorbed
amount in four of the subjects and 5.1% in a fifth subject. It is not evident whether these datafor ingestion of biologically incorporated polonium are pertinent to occupational exposures to210
Po, but the data demonstrate the potentially high absorption of some forms of polonium
from the GI tract and the potentially high variability in the biokinetics of absorbed polonium.
Laboratory animals
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7741
7742
7743
7744
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7746
7747
7748
7749
7750
7751
7752

7753
7754
7755
7756
7757

(576) Data on the biokinetics of polonium in laboratory animals was reviewed by Leggett
and Eckerman (2001). The systemic behavior of polonium is qualitatively similar among
species in most respects, but some species differences have been identified. For example, theblood cells of rats appear to have an unusually high affinity for polonium absorbed afteringestion, and rabbits show an unusually high rate of loss of polonium from the body.
11.2.3.2. Biokinetic model for systemic polonium(577) A biokinetic model for systemic polonium proposed by Leggett and Eckerman(2001) is used in this report. The model structure is shown in Figure 11-1. Transfer
coefficients are given in Table 11-3. The basis for each of the transfer rates is discussed
below.

Figure 11-1. Structure of the biokinetic model for systemic polonium.

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7759
7760
7761

Table 11-3. Transfer coefficients in the model for systemic polonium.

From
Plasma 2
Plasma 2
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 3
RBC
Liver 1
Liver 2Kidneys 1
Kidneys 2
Skin
Skin
Red Marrow
Bone Surface
SpleenGonads
Other
7762
7763
7764
7765
7766
7767
7768
7769
7770
7771
7772
7773
7774
7775
7776
7777

To
Plasma 1
Kidneys 1
Plasma 3
RBC
Liver 1
Liver 2Kidneys 1
Kidneys 2
Skin
Red Marrow
Bone Surface
SpleenTestesOvaries
Other
Plasma 1
Plasma 1
GI Tract
Plasma 1
Urinary Bladder
Plasma 1
Plasma 1
Excreta
Plasma 1
Plasma 1
Plasma 1
Plasma 1
Plasma 1

Transfercoefficient (d-1)
800
200
4
6
17.5
17.5
5
5
5
4
1.5
2
0.1
0.05
32.35
0.099
0.099
0.139
0.099
0.173
0.099
0.00693
0.00693
0.099
0.0231
0.099
0.01390.099

Blood(578) Data on non-human primates indicate that there is a rapid phase of removal ofpolonium from blood, followed by one or more slower phases of removal (Cohen et al.,1989). The rapid phase represented about 80-90% of intravenously injected polonium andhad a half-time on the order of 10-40 min. The remainder was removed with a half-time ofabout 8-19 d in the baboon and about 37 d in the tamarin. The slower phase of removal
appears to be associated with attachment of polonium to red blood cells and plasma proteins(Thomas 1964, Cohen et al., 1989).
(579) The relative quantities of polonium associated with red blood cells and plasma
proteins varies with species, but in all species the total amount of polonium in red blood cells
exceeds that in plasma at most times after absorption or injection of polonium into blood(Silberstein et al., 1950a; Smith et al., 1961; Thomas, 1964; Cohen et al., 1989). There wasconsiderable inter- and intra-subject variability in the relative quantities of 210Po in red blood
cells and plasma determined in human subjects administered 210Po by intravenous injection oringestion, but the content of red blood cells averaged about 1.5 times that of plasma

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7779
7780
7781
7782
7783
7784
7785
7786
7787
7788
7789
7790
7791
7792
7793
7794
7795
7796
7797
7798
7799
7800
7801
7802
7803
7804
7805
7806
7807
7808
7809
7810
7811
7812
7813
7814
7815
7816
7817
7818
7819
7820
7821
7822

(Silberstein et al., 1950b).
(580) The initial behavior of polonium in blood may depend on the route of exposure.
After exposure by inhalation or wounds there is generally an early, rapid loss of polonium in
urine (Foreman et al., 1958; Smith et al., 1961; Casarett, 1964; Wraight and Strong, 1989)
that appears to be absent or less pronounced after exposure by other routes.
(581) The model for blood was designed to depict rapid and slow phases of removal suchas those observed in non-human primates (Cohen et al., 1989); to approximate blood
retention data for human subjects (Silberstein et al., 1950a), non-human primates (Cohen etal., 1989, Fellman et al., 1994), and dogs (Parfenov and Poluboyarinova, 1969); and to depict
a higher rate of urinary excretion of polonium after exposure through inhalation or wounds
than after exposure by other routes. Variation in the rate of urinary excretion with route of
exposure is modelled by using different receptor compartments in plasma with different ratesof transfer to the urinary excretion pathways. Specifically, a compartment called Plasma 2 isassumed to receive inflow to blood from the respiratory tract or wounds, and a compartment
called Plasma 1 is assumed to receive inflow to blood from all other sources, including
polonium that returns from systemic tissues to blood. Outflow from Plasma 2 is assumed to
be rapid (half-time of 1 min, corresponding to a transfer rate of 1000 d-1) and is divided
between Plasma 1 and a kidney compartment (Kidneys 1) that feeds the urinary bladdercontents. This scheme yields an initially higher rate of urinary excretion for exposure byinhalation or wounds than for other routes. As default values, 80% of outflow from Plasma 2
is assigned to Plasma 1 and 20% is assigned to Kidneys 1. Assignment of a higher percentage
to Kidneys 1 may be indicated in cases where the observed urinary excretion rate falls rapidly
during the first few days after acute intake of polonium. This is because an unusually rapid
decline in the urinary excretion rate may indicate that an unusually high fraction of theamount entering the systemic circulation was rapidly cleared by the kidneys.
(582) A third plasma compartment, called Plasma 3, is used to represent protein-bound, or
non-diffusible polonium in plasma. Red blood cells are represented by a single compartment,
called RBC.
(583) The removal half-time from Plasma 1 is assumed to be 10 min, corresponding to a
total transfer rate of 100 d-1. Plasma 3 is assumed to receive 4% and RBC is assumed toreceive 6% of the polonium atoms that leave Plasma 1 (i.e. the deposition fractions for
Plasma 3 and RBC are 0.04 and 0.06, respectively). The removal half-time from either RBC
or Plasma 3 back to Plasma 1 is assumed to be 7 d. The term half-time refers here to theestimated half-time that would be seen if there were no recycling of polonium between
compartments, and that the “apparent” or “externally viewed” half-time in blood will begreater than 7 d due to recycling of polonium.
Liver and faecal excretion(584) Data for laboratory animals (Smith et al., 1961; Parfenov and Poluboyarinova, 1969,
Fellman et al., 1994) and one human subject (Silberstein et al., 1950b) indicate that asubstantial portion of injected or absorbed polonium deposits in the liver. It appears thatmuch of the initial uptake by the liver may be removed with a half-time of a few days, and theremainder may be lost over a period of weeks. Endogenous fecal excretion of polonium
appears to arise mainly from biliary secretion from the liver (Silberstein et al., 1950b;
Fellman et al., 1994).

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7824
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7829
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7831
7832
7833
7834
7835
7836
7837
7838
7839
7840
7841
7842
7843
7844
7845
7846
7847
7848
7849
7850
7851
7852
7853
7854
7855
7856
7857
7858
7859
7860
7861
7862
7863
7864
7865
7866
7867
7868
7869
7870

(585) In this model the liver is assumed to consist of two compartments, called Liver 1 andLiver 2. Liver 1 is used to represent relatively rapid removal of polonium from the liver andto account for biliary secretion of polonium, which appears to decline rapidly with time.
Liver 2 is used to describe relatively long-term retention in the liver.
(586) The total liver is assumed to receive 35% of the outflow from Plasma 1, with half of
this amount depositing in Liver 1 and half depositing in Liver 2. Polonium is assumed to be
removed from Liver 1 to the contents of the small intestine with a half-time of 5 d and from
Liver 2 to Plasma 1 with a half-time of 7 d. Passage from Plasma 1 to Liver 1 to the contentsof the small intestine is assumed to be the sole source of endogenous fecal excretion ofpolonium.
Kidneys and urinary excretion(587) In this model the kidneys are assumed to consist of two compartments, called
Kidneys 1 and Kidneys 2. Kidneys 1 represents polonium that is eventually removed to theurinary bladder contents after filtration at the glomerulus and deposition in the renal tubules.
Kidneys 2 represents polonium that is eventually returned to blood after entering kidney
tissue, either from nutrient blood or the tubular lumen. For simplicity, polonium entering
either Kidneys 1 or Kidneys 2 is assumed to transfer directly from Plasma 1. Also, there isassumed to be no direct transfer of filtered polonium into the urinary bladder contents. Thatis, filtered polonium is assumed to reside temporarily in kidney tissue before being transferredto the urinary bladder contents.
(588) Parameter values describing renal retention of polonium were chosen to fit retention
data for man, baboons, and dogs. Kidneys 1 and Kidneys 2 are each assumed to receive 5%of polonium atoms that leave Plasma 1. The removal half-time from Kidneys 1 to bladderurine is assumed to be 4 d, and the removal half-time from Kidneys 2 to Plasma 1 is assumed
to be 7 d.
(589) After parameter values describing fecal excretion of polonium had been selected,
parameter values describing urinary excretion were set, in part, to yield a (cumulative) fecalto-urinary excretion ratio, F:U, of about 3. The typical value of F:U for man has not been
established. The selected value of 3 is a compromise, based on a fairly wide range of values
determined for human subjects and non-human primates. The selected value is slightly lower
than the value determined for tamarins (Cohen et al., 1989; Fellman et al., 1989) and higher
than the value determined for baboons (Fellman et al., 1989). The true ratio seems likely to
be lower than the values of 10 or more determined by Silberstein et al. (1950b) for humansubjects, in view of findings of Fellman et al. (1989) that the measurement technique ofSilberstein substantially underestimates the concentration of polonium in urine, at least inbaboons and tamarins. Results of a modern study on a human subject exposed through apuncture wound seem consistent with the relatively low urinary-to-fecal excretion ratio
determined by Silberstein and coworkers (Wraight and Strong, 1989); however, the techniquefor measuring urinary polonium was not described, and conclusions concerning F:U werebased on an uncertain curve fit to scattered fecal excretion data. Reported ratios F:U forhuman subjects exposed to 210Po by inhalation are in the range 6.5-70 but provide only upperbound estimates of F:U for systemic polonium, for two reasons: (1) a substantial portion of210
Po found in faeces may have been transported from the lungs to the gastrointestinal tract
without having been absorbed to blood; and (2) at least some of the reported values werebased on a measurement technique that may substantially underestimate the concentration of210
Po in urine.
(590) The measurement technique used by Silberstein et al. (1950b) and some later
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7871
7872
7873
7874
7875
7876
7877
7878
7879
7880
7881
7882
7883
7884
7885
7886
7887
7888
7889
7890
7891
7892
7893
7894
7895
7896
7897
7898
7899
7900
7901
7902
7903
7904
7905
7906
7907
7908
7909
7910
7911
7912
7913
7914
7915
7916
7917
7918

investigators involved spontaneous deposition of 210Po from raw urine onto a suitable metal
disc. Recovery was estimated by plating 210Po from samples that had been spiked withknown amounts of 210Po. There is evidence from studies on laboratory animals, however,that 210Po excreted in urine is not plated with the same efficiency as 210Po added to urine,
unless the samples have been digested with acid prior to deposition (Fellman et al., 1989).
Although it is tempting to adjust older urinary excretion data for human subjects to accountfor potentially low recovery of 210Po as indicated by results for laboratory animals, suchadjustments would involve substantial uncertainties because recovery of metabolized 210Po
from raw urine appears to depend on species as well as time since exposure (Fellman et al.,1989), and because there is some question as to whether inaccuracies in older methods are as
great as indicated by modern reconstructions of those methods. Moreover, reported data on
urinary excretion of 210Po often have not been accompanied by a description of themeasurement technique.
Spleen(591) The spleen is represented as a single compartment in exchange with Plasma 1.
Parameter values were set for reasonable consistency with spleen retention data for baboons,dogs, and one human subject (Leggett and Eckerman, 2001). It is assumed that the spleen
receives 2% of the outflow from Plasma 1 and that the removal half-time from spleen to
Plasma 1 is 7 d.
Skin(592) Data on laboratory animals and man indicate that skin initially takes up a few percent
of polonium that enters plasma but retains polonium more tenaciously than most other tissues.
At times remote from acute intake, skin may contain half or more of the systemic burden.
Much of the skin content is found around hair follicles (Soremark and Hunt 1966). Hair has arelatively high polonium content at times remote from exposure (Mayneord and Hill 1964).
(593) In this model, skin is represented as a single compartment that receives 5% ofpolonium that leaves Plasma 1. The removal half-time from skin is assumed to be 50 d. Halfof polonium leaving skin is assumed to be lost in excreta (hair, skin, sweat) and the other half
is assumed to return to Plasma 1.
(594) In baboons, pelt contained 53% of the body content at 91 d post injection (Fellman etal., 1989). In dogs, the pelt contained 44%, 43%, 54% and 51% of total-body polonium at
116, 131, 146, and 149 d after inhalation (Smith et al., 1961). Model predictions arereasonably consistent with these data.
Skeleton(595) Experimental data on laboratory animals indicate that about 5% of the injected orabsorbed amount deposits in the skeleton. Soon after exposure, most of the skeletal
deposition is found in the marrow spaces and appears to be associated primarily with active
marrow (ICRP, 1993). A smaller amount found in the mineralized skeleton may be
associated with organic material in bone. The bone deposit may be retained longer than mostsoft-tissue polonium.
(596) In this model, the skeleton is represented as two compartments, identified with red
marrow and bone surface. It is assumed that these compartments receive, respectively, 4%
and 1.5% of polonium leaving Plasma 1, and that both compartments lose polonium to
Plasma 1. The removal half-time from red marrow is assumed to be 7 d, and the removal
half-time from bone surface is assumed to be 30 d.
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7919
7920
7921
7922
7923
7924
7925
7926
7927
7928
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7930
7931
7932
7933
7934
7935
7936
7937
7938
7939
7940
7941
7942
7943
7944
7945
7946
7947
7948
7949
7950
7951
7952
7953
7954
7955
7956
7957
7958
7959
7960
7961
7962
7963
7964
7965
7966

Gonads(597) Data on uptake and retention of polonium by testes or ovaries are variable but
indicate elevated concentrations compared with most tissues (Silberstein et al., 1950b,
Blanchard and Moore 1971; Cohen et al., 1989; Naylor et al., 1991). In this model, the testes
and ovaries are each considered as a single compartment that exchanges polonium with
Plasma 1. These compartments are assumed to receive, respectively, 0.1% and 0.05% ofpolonium leaving Plasma 1. The removal half-time from each of these compartments is
assumed to be 50 d.
Other tissues(598) Remaining tissues and fluids are lumped into a compartment called Other that isassumed to exchange polonium with Plasma 1. Parameter values for this compartment werechosen for consistency with data on baboons (Cohen et al., 1989). Other is assumed toreceive 32.35% of polonium leaving Plasma 1, which is the amount not accounted for in thesum of deposition fraction for all explicitly identified compartments. The removal half-timefrom Other to Plasma 1 is assumed to be 7 d.
11.2.3.3. Treatment of radioactive progeny(599) Dosimetrically significant progeny of polonium isotopes addressed in this report areisotopes of bismuth or lead. The models for these two elements produced in systemiccompartments following intake of a polonium isotope are based on their characteristic
models, i.e. the systemic models applied in this series of reports to bismuth and lead as parent
radionuclides.
(600) For application to bismuth and lead as progeny of polonium, the characteristic
models for bismuth and lead are modified by adding compartments representing the following
tissues that are explicitly identified in the polonium model: spleen, skin, red marrow, testes,and ovaries. The model revisions are similar for each element and are summarized here forbismuth. Each of these tissues is represented in the bismuth model as a single compartment.
The five compartments are extracted from the intermediate- and long-term compartments of
Other soft tissues (ST1 and ST2, respectively). Transfer coefficients between the added
compartments and the central blood compartment are based on the biokinetic database forbismuth summarized elsewhere in this series of reports, together with the requirements thatthe total outflow rate of bismuth from blood and integrated activities of long-lived bismuth
isotopes in total soft tissues remain unchanged from the characteristic model for bismuth(except for small changes due to rounding of parameter values).
(601) The specific changes to the characteristic model for bismuth are as follows: (1) thetransfer coefficient from the central blood compartment (plasma) to ST1 is reduced from 4.2
d-1 to 3.7 d-1, and the coefficient from plasma to ST2 is reduced from 1.3 d-1 to 1.2 d-1; (2) the
following transfer coefficients from plasma to the added compartments are assigned: to Red
marrow, 0.3 d-1, to Spleen, 0.02 d-1, to Skin, 0.3 d-1, to Testes, 0.003 d-1, to Ovaries, 0.001 d-1;
(3) the assigned transfer coefficient from Red marrow, Spleen, Skin, Testes, and Ovaries toplasma is 0.007 d-1; and (4) the following transfer coefficients are assigned to bismuth
produced in compartments of the polonium model that are not identifiable with compartmentsof the bismuth model: Plasma 2 to the plasma compartment of the bismuth model, 1000 d-1;
Plasma 3 to the plasma compartment of the bismuth model, 1000 d-1; and Other to the plasmacompartment of the bismuth model, 0.0347 d-1 (based on removal rate from ST1 to plasma in
199

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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7968
7969
7970
7971
7972
7973
7974
7975
7976
7977
7978
7979
7980
7981
7982
7983
7984
7985
7986
7987
7988
7989
7990
7991

7992
7993
7994
7995
7996
7997
7998
7999
8000
8001
8002
8003
8004
8005
8006
8007
8008
8009
8010

the model for bismuth).
(602) The specific changes to the characteristic model for lead are as follows: (1) thetransfer coefficient from the central blood compartment (Plasma) to ST1 is reduced from 0.70
d-1 to 0.65 d-1, and the coefficient from Plasma to ST2 is reduced from 0.14 d-1 to 0.13 d-1; (2)the following transfer coefficients from Plasma to the added compartments are assigned: to
Red marrow, 0.015 d-1, to Spleen, 0.002 d-1, to Skin, 0.04 d-1, to Testes, 0.00045 d-1, toOvaries, 0.00015 d-1; (3) the assigned transfer coefficient from Red marrow, Spleen, Skin,
Testes, and Ovaries to Plasma is 0.002 d-1; and (4) the following transfer coefficients are
assigned to lead produced in compartments of the polonium model that are not identifiablewith compartments of the lead model: Plasma 2 to Plasma, 1000 d-1; Plasma 3 to Plasma,1000 d-1; Other to Plasma, 0.00416 d-1 (based on removal rate from ST1 to Blood 1 in themodel for lead).
(603) For modelling convenience, the compartment in the polonium model named Plasma
1 is identified with the compartment in the bismuth model named Plasma and thecompartment in the lead model named Plasma. For example, a bismuth atom produced in
Plasma 1 is assumed to be produced in the plasma compartment of the bismuth model, and alead atom produced in Plasma 1 is assumed to be produced in the plasma compartment of thelead model.
11.3.

Individual monitoring

210Po(604) Monitoring of 210 Po intakes is accomplished through urine bioassay, using atechnique that involves wet acid digestion followed by alpha spectrometry.
IsotopeMonitoring
Technique

210

Urine Bioassay

Po

MethodMeasurementof Typical
DetectionLimitalpha spectrometry 1 mBq/L

Achievabledetection limit
0.1 mBq/L

References
Anthony, D.S., Davis, R.K., Cowden, R.N., Jolley, W.P., 1956. Experimental data useful inestablishing maximum single and multiple exposure to polonium. In: Proceedings of theInternational Conference on the Peaceful Uses of Atomic Energy, Vol. 13, pp.215-218.
United Nations, New York.
Bailey, M.R., Hodgson, A., Smith, H., 1985. Respiratory tract retention of relatively insoluble
particles in rodents. J. Aerosol Sci., 16, 279–293.
Berke H.L., Dipasqua A.C. 1957. The distribution and excretion of polonium210 after inhalation.
University of Rochester Atomic Energy Project, Report UR-495.
Berke, H.L., Dipasqua, A.C., 1964. Distribution and excretion of polonium-210. VIII. Afterinhalation by the rat. Radiat Res 5 (suppl.), 133-147.
Blanchard, R.L., Moore, J.B., 1971. Body burden, distribution and internal dose of Pb-210 and Po210 in a uranium miner population. Health Phys. 21, 499-518.
Borisov, N.B., 1999. On the 275th Anniversary of the Russian Academy of Sciences, Research onpolonium aerosols and appropriate safety measures under the leadership of I. V. PetryanovSokolov. Atomic Energy. 86 (6) 385–387.

200

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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8012
8013
8014
8015
8016
8017
8018
8019
8020
8021
8022
8023
8024
8025
8026
8027
8028
8029
8030
8031
8032
8033
8034
8035
8036
8037
8038
8039
8040
8041
8042
8043
8044
8045
8046
8047
8048
8049
8050
8051
8052
8053
8054
8055
8056
8057
8058
8059
8060
8061

Casarett, L.J. 1958. A study of the pharmacodynamics of polonium administered via the lungs. PhD
Thesis, University of Rochester.
Casarett, L.J. 1964. Distribution and excretion of polonium-210. IX. Deposition, retention, and fateafter inhalation by nose-only exposure, with notes on mechanics of deposition and clearance
and comparison of routes of administration. Radiat Res 5 (suppl.), 148-165.
Chu, K.-D., Hopke P.K., 1988. Neutralization kinetics for polonium-218. Environ. Sci. Technol., 22,711-717.
Cohen, B.S., Eisenbud, M., Wrenn, M.E., Harley, N.H., 1979. Distribution of polonium-210 in thehuman lung. Radiat. Res. 79, 162-168.
Cohen, N., Fellman, A.L., Hickman, D.P., Ralston, L.G., Ayres, L.S., 1989. Primate polonium
metabolic models and their use in estimation of systemic radiation doses from bioassay
data. Mound Laboratory.
Cohen,B.S., Eisenbud, M., Harley, N.H., 1980. Alpha Radioactivity in cigarette smoke. Radiat Res
83, 190-196.
Cohen, B.S., Harley, N.H., Tso,T.C., 1985. Clearance of polonium-210-enriched cigarette smokefrom the rat trachea and lung. Toxicol. Appl. Pharmacol. 79, 314-322.
Cross F.T., 1984. Radioactivity in cigarette smoke issue. Health Phys. 46(1) 205-209.
Della Rosa, J.R., Thomas, R.G., Stannard, J.N., 1955. The acute toxicity and retention of orally
administered polonium-210. University of Rochester, UR-392.
Desideri D., Meli M.A., Feduzi L., Roselli, C., 2007. 210Po and 210Pb inhalation by cigarette smoking
in Italy. Health Phys. 92(1) 58-63.
Fellman, A., Ralston, L., Hickman, D., Ayres, L., Cohen, N., 1994. Polonium metabolism in adultfemale baboons. Radiat. Res. 137, 238-250.
Fellman, A., Ralston, L., Hickman, D., Ayres, L., Cohen, N., 1989. The importance of acid digestionof urine prior to spontaneous deposition of 210Po. Health Phys. 57, 615-6221.
Fink, R.M., 1950. (Ed.), Biological studies with polonium, radium, and plutonium. New York:
McGraw-Hill.
Foreman, H., Moss, W., Eustler, B.C., 1958. Clinical experience with radioactive materials.
American Journal of Roentgenology Radium Therapy and Nuclear Medicine 79, 10711079.
Haines, J.W., Naylor, G.P.L., Pottinger, H., Harrison, J.D., 1993. Gastrointestinal absorption andretention of plonium in adult and newborn rats and guinea pigs. Int. J. Radiat. Biol. 64, 127132.
Harrison, J.D., Leggett, R.W., Lloyd D., Phipps, A.W., Scott, B.R., 2007. Polonium-210 as a poison.
J. Radio. Prot. 27, 17–40.
Holtzman, R.B., Ilcewicz, F.H., 1966. Lead-210 and polonium-210 in tissues of cigarette smokers.
Sci. 153, 1259-1260.
Holtzman, R.B., 1967. Polonium-210 in bronchial epithelium of cigarette smokers. Sci. 155, 607.
Hunt, G.J., Allington, D.J., 1993. Absorption of environmental polonium-210 by the human gut. J.
Radiol. Prot. 13, 119-126.
ICRP, 1975. Report of the Task Group on Reference Man. ICRP Publication 23. Oxford: Pergamon
Press.
ICRP, 1979. Limits on Intakes of Radionuclides for Workers. ICRP Publication 30, Pt.1. Ann. ICRP
2, (3/4).
ICRP, 1993. Age-dependent Doses to Members of the Public from Intake of Radionuclides. Pt.2.
ICRP Publication 67. Ann. ICRP. 23, (3/4).
Ilyin, L.A., 2001. Radiation Medicine. Guidance for Medical Researchers and Health Management.
Vol 2. Radiation Damage of Humans. Ed. A. Yu. Bushmanov et al. (Moscow: AT) ISBN 586656-114-X.
Jackson, S., Dolphin, G.W., 1966. The estimation of internal radiation dose from metabolic andurinary excretion data for a number of important radionuclides. Health Phys. 12, 481-500.

201

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
8062
8063
8064
8065
8066
8067
8068
8069
8070
8071
8072
8073
8074
8075
8076
8077
8078
8079
8080
8081
8082
8083
8084
8085
8086
8087
8088
8089
8090
8091
8092
8093
8094
8095
8096
8097
8098
8099
8100
8101
8102
8103
8104
8105
8106
8107
8108
8109
8110
8111
8112
8113

Kalkwarf, D.R., Jackson, P.O., 1984. Lung-clearance classification of radionuclides in calcined
phosphate rock dust. PNL-5221.. Richland, Washington, Pacific Northwest Laboratory.
Kalkwarf, D.R., Jackson, P.O., Hardin, J.M., 1984. Lung-clearance classification of radionuclides incoal fly ash. Health Phys. 47, 37-45.
Kimball, C.P., Fink, R.M., 1950. Inhalation of volatilized polonium by rats. In: Fink, R.M., editor.
Biological studies with polonium, radium, and plutonium. New York: McGraw-Hill, pp.
89–111.
Landinskaya, L.A., Parfenov, Y.D. Popov, D.K., Federova, A.V., 1973. 210Pb and 210Po content of air,weater, foodstuffs and the human body. Arch. Environ. Health 27, 254-258.
Leggett, R.W., Eckerman, K.F., 2001. A systemic biokinetic model for polonium. Sci. Total Environ.
275, 109-125.
Little, J.B., Radford, E.P., Jr. 1967. Polonium-210 in bronchial epithelium of cigarette smokers. Sci.
155, 606-607.
Little, J.B., Radford, E.P., Jr., McCombs, H.L., Hunt, V.R., 1965. Distribution of polonium-210 inpulmonary tissues of cigarette smokers. N. Engl. J. Med. 273, 1343-1351.
Martell, E.A. 1974. Radioactivity of tobacco trichomes and insoluble cigarette smoke particles.
Nature 249, 215-217.
Mayneord, W.V., Hill, C.R., 1964. Total counting and spectroscopy in the assessment of alphaactivity in human tissues. In: Assessment of radioactivity in man, Vol. 1. IAEA, Vienna,
Austria, 291-309.
Morrow, P.E., Della Rosa, R.J., 1956. The fate of polonium210 colloid and polonium210 tagged silver
particles following intratracheal administration to rabbits. University of Rochester Atomic
Energy Project, Report UR-478.
Morrow, P.E., Della Rosa, R.J., 1964. Distribution and excretion of polonium-210. VII. Fate ofpolonium colloid after intratracheal administration to rabbits. Radiat Res 5 (suppl.), 124132.
Morrow, P.E., Della Rosa, R.J., Casarrett L.J., Miller, G.J., 1964. Investigations of the colloidal
properties of polonium-210 solutions using molecular filters. Radiat Res 5 (suppl.), 1-15.
Naimark, D.H., 1948. Acute exposure to polonium (medical study of three human cases). MoundLaboratory, Report MLM-67.
Naimark, D.H. 1949. Effective half-life of polonium in the human. Mound Laboratory, Report MLM272.
Naylor, G.P.L., Bonas, H.E., Haines, J.W., Ham, G.J., Harrison, J.D., Sundaram, S., Dayan, A.D.,
1991. The gastrointestinal absorption and tissue distribution of alpha-emitting actinide
isotopes and polonium-210. The British Nuclear Energy Society Conference: Occupational
Radiation Protection, Guernsey. Thomas Telford, London. 291-296.
Parfenov, Y. 1974. Polonium-210 in the environment and in the human organism. At. Energy Rev.
12, 75-143.
Parfenov, Yu. D., Poluboyarinova, Z.I., 1969. Dynamics of polonium-210 exchange in dogs after asingle subcutaneous administration. Radioactive isotopes and the body, Yu. I. Moskaleve,ed. Izdatel’stvo Medisina. Moscow. 1969. AEC-tr-7195, pp. 128-135.
Radford, E.P., Martell, E.A., 1975. Polonium-210: lead-210 ratios an index of residence times of
insoluble particles from cigarette smoke in bronchial epithelium. Walton, W.H. andMcGovern, B. 2, 567-581. 1975. Oxford, Pergamon Press. Proc. of an international
symposium organized by the British Occupational Hygiene Society, Edinburgh. 22-9-1975.
Rajewsky, B., Stahlhofen, W., 1966. Polonium-210 activity in the lungs of cigarette smokers. Nature
209, 1312-1313.
Scott, B.R., 2007. Health risk evaluations for ingestion exposure of humans to polonium-210. Dose
Response 5: 94-122;
Scott, L.M., West, C.M., 1975. Excretion of 210-Po oxide following accidental inhalation. HealthPhys. 28, 563-565.
Sheehan, W.E., 1964. Effective half-life of polonium. Proc. 10th annual bioassay and analytical202

DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
8114
8115
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8137
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8141
8142
8143
8144
8145
8146
8147
8148
8149
8150
8151
8152
8153

chemistry meeting. Conf. 727, pp. 32-38.
Silberstein, H.E., Minto, W.L., Fink, R.M. 1950a. Intravenous injection of polonium in a rabbit. In:
Biological Studies With Polonium, Radium and Plutonium (Ed. by R.M. Fink), pp. 117-119.
New York, McGraw-Hill.
Silberstein, H.E., Valentine, W.N., Minto, W.L., Lawrence, J.S. & Fink, R.M. 1950b. Studies ofpolonium metabolism in human subjects. Intravenous studies, comparison of intravenous
studies, oral administration. In: Fink, R.M. (Ed.), Biological Studies With Polonium,
Radium and Plutonium, pp. 122-148. New York, McGraw-Hill.
Silverman, L.B., 1994. Excretion activity analyses as a monitor for postum exposures. Final report
No. 10. Mound Laboratory. MLM-1443. Miamisburg, Ohio.
Skwarzec, B., Ulatowski, J., Struminska, D.I., Borylo, A., 2001. Inhalation of 210Po and 210Pb fromcigarette smoking in Poland. J. Environ. Radioact. 57, 221-230.
Smith, F.A., Morrow, P.E., Gibb, F.R., Della Rosa, R.J., Casarett, L.J., Scott, J.K., Morken D.A. andStannard, J.N. 1960. Distribution and excretion studies in dogs exposed to an aerosol
containing polonium-210. University of Rochester Atomic Energy Project, Report UR-566.
Smith, F.A., Morrow, P.E., Gibb, F.R., Della Rosa, R.J., Casarett, L.J., Scott, J.K., Morken, D.A.,
Stannard, J.N. 1961. Distribution and excretion studies in dogs exposed to an aerosol
containing polonium-210. Am. Ind. Hyg. Assoc. J. 22, 201-208.
Soremark, R., Hunt, V.R., 1966. Autoradiographic studies of the distribution of polonium-210 inmice after a single intravenous injection. Int. J. Rad. Biol. 11, 43-50.
Spoerl, E., Anthony, D.S. 1956. Biological research related to polonium. In : Polonium. United States
Atomic Energy Commission Technical Information Service Extension, July 1956, Oak
Ridge, TN.
Spoerl, E.S., 1951. A derived biological half-life of polonium in humans. Mound Laboratory, MLM626. Report for biological research, 72-76.
Stannard, J.N., 1964. Distribution and excretion of polonium-210. I. Comparison of oral andintravenous routes in the rat. Radiat. Res. 5 (suppl.), 49-59.
Testa, C., 1972. Indirect methods used at CNEN for the evaluation of internal contamination. In:
Assessment of radioactive contamination in man. IAEA-SM-150/18, Vienna, pp. 405-421.
Thomas, R.G., 1964. The binding of polonium by red cells and plasma proteins. Radiat. Res. Suppl.
5, 29-39.
Thomas, R.G., and Stannard, J.N., 1956. The metabolism of polonium-210 administered byintratracheal injection to the rat. University of Rochester Atomic Energy Project, Report
UR-430.
Thomas, R.G., Stannard, J.N., 1964. Distribution and excretion of polonium-210. VI. After
intratracheal administration in the rat. Radiat. Res. 5 (suppl.), 106-123.
Wraight, J.C., Strong, R.A., 1989. Case study on the retention and excretion of internally depositedpolonium. Radiation protection - theory and practice. Proc. of the 4th International
Symposium, Malvern, pp 227-230.

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8162
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8164
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8166
8167
8168
8169
8170

12.
12.1.

Radon (Z = 86)

Chemical forms in the workplace(605) Radon is an inert (noble) gas that is encountered in elemental form either as a gas, ordissolved, usually in water.
(606) Three isotopes of radon are considered in this section, 222Rn, 220Rn and 219Rn (Table
12-1). They are usually encountered as decay products of radium isotopes (226Ra, 224Ra and223Ra), which are members of the three natural radioactive decay series, headed by theprimordial radionuclides 238U, 232Th and 235U respectively (Figures 12-1 to 12-3). Because of
their origins, the isotopes 222Rn, 220Rn, 219Rn are commonly known as radon, thoron andactinon respectively. The two isotopes 222Rn and 220Rn are the main sources of exposure
from radon of importance for radiation protection.
Table 12-1. Isotopes of radon addressed in this report
IsotopeRn-222 (radon)
Rn-220 (thoron)
Rn-219 (actinon)

Physical half-life
3.8 days
56 seconds
4.0 seconds

Decay mode
Alpha
Alpha
Alpha

8171

8172
8173
8174
8175

Figure 12-1. Natural decay series: Uranium-238

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Notes:The symbols α and β indicate alpha and beta
decay, and the times shown are half-lives.

Uranium-235*α

700 million years

An asterisk indicates that the isotope is also
a significant gamma emitter.

Protactinium-231*βα33,000 years

26 hours
Thorium-227*

Thorium-231

βActinium-227
α

22 years(99%)α

19 daysRadium-223*
22 yearsαβ
11 days(1%)
22 minutes

Francium-223*

Radon-219*
α4.0 seconds

Polonium-215
α

1.8 milliseconds
Bismuth-211*β

α2.1 minutes

36 minutes

Lead-211*

Lead-207 (stable)
β4.8 minutes

Thallium-207

8176
8177
8178
8179

Figure 12-2. Natural decay series: Uranium-235

8180
8181
8182

Figure 12-3. Natural decay series: Thorium-232

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8200
8201
8202
8203
8204
8205
8206
8207
8208
8209
8210

(607) Uranium, radium and thorium occur naturally in soil and rocks and provide acontinuous source of radon. Radon can escape from the Earth's crust either by molecular
diffusion or by convection and as a consequence is present in the air outdoors and in allbuildings including workplaces. The build up of activity concentrations of radon and its
short-lived decay products within enclosed spaces gives rise to a radiation hazard. Thisapplies particularly to workplaces such as underground mines, tourist caves, and water supply
facilities where ground water with a high radon concentration is treated or stored.
(608) In general the problems posed by radon (222Rn) are much more widespread thanthose posed by thoron (220Rn). Because thoron (220Rn) has a short half-life (56 s), it is lessable than radon (222Rn) to escape from the point where is formed. As a consequence, building
materials are the most usual source of indoor thoron exposure. In contrast, radon (222Rn),
which has a half-life of 3.8 days can diffuse in soil more than a meter from the point where it
is formed. As a result the ground underneath buildings is usually the main source of indoor
radon (222Rn). Because actinon (219Rn) has an even shorter half-life (4 s) its contribution to
workplace exposure is generally low and in most situations can be ignored. Dose coefficientsfor it and its short-lived decay products are discussed in Section 12.5.4.
(609) Radon (222Rn), thoron (220Rn) and actinon (219Rn) gases decay into a series of solid
short-lived radioisotopes (Figures 12-1 to 12-3). The resulting aerosol is created in two steps(Figure 12-4). After decay of the radon gas, the freshly formed radionuclides react rapidly (<1 s) with trace gases and vapours and grow by cluster formation to form particles around 1
nm in size. These are referred to as unattached progeny. The unattached radionuclides may
also attach to existing aerosol particles in the atmosphere within 1 – 100 s forming the socalled attached progeny. The attached progeny can have a trimodal activity size distribution
which can be described by a sum of three lognormal distributions (Porstendörfer, 2001).
These comprise the nucleation mode with an activity median thermodynamic diameter(AMTD) between 10 nm and 100 nm, the accumulation mode with AMTD values of 100 –450 nm and a coarse mode with activity median aerodynamic diameter, AMAD > 1 μm.
Generally, the greatest activity fraction is in the accumulation mode.

8211
8212
8213

Figure 12-4. Schematic representation of the behaviour of radon progeny in an enclosed space,(NRC, 1991; Porstendörfer, 1994)

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8223
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8232
8233
8234
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8239
8240
8241
8242
8243
8244
8245
8246
8247
8248
8249
8250
8251
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8253

(610) Because radon progeny in the air can be removed by plate-out (i.e. by deposition on
surfaces) and ventilation, the activity concentrations of the short-lived radon progeny in the
air are less than that of the radon gas. This is quantified by the equilibrium factor, F which isa measure of the degree of disequilibrium between the radon gas and its progeny (see below).
If the activity concentrations of the short-lived radon progeny were equal to the activity
concentration of the radon gas (i.e. secular equilibrium had been reached) then F would be 1.
However, because of plate-out and ventilation, F is in practice always less than 1; typicallyfor 222Rn, F is 0.4 for indoor air and 0.2 for force-ventilated mines.
(611) For exposures to radon (222Rn) and thoron (220Rn) gas, inhalation of their short-lived
decay products generally gives much higher contributions to effective dose than inhalation of
the gas itself (Figures 12-1 to 12-3). Following inhalation of the short-lived progeny most of
their decay takes place in the lung before clearance can occur, either by absorption into blood
or by particle transport to the alimentary tract. As a consequence the lung dose contributes
more than 95% of the effective dose. Because of the importance of this route of exposure,detailed consideration is given below to exposures to radon and thoron decay products.
Exceptionally, dose coefficients are given here for simultaneous intakes of radon with its
short-lived decay products, under exposure conditions representative of two different types of
workplace.
12.2.

Special quantities and units(612) Special quantities and units are used to characterise the concentration of radon andits short-lived progeny in the air, and the resulting inhalation exposure.
Concentration(613) The dose to the lung mainly arises from the inhalation of the short-lived radon
progeny and the alpha particles emitted during their decay and that of their short-lived
progeny. The quantity ‘potential alpha energy concentration (PAEC)’ of the radon progeny
mixture was historically used as a measure of concentration that was an indicator of dose andrisk. The potential energy, εp,i of an atom, i, in the decay chain of radon (222Rn) is the totalalpha energy emitted during the decay of this atom to stable 210Pb. The PAE per unit ofactivity (Bq) of radionuclide, i, is εp,i / λr,i where λr (in s-1) is the radioactive decay constant.
The PAE per atom and per unit activity are listed in Table 12-2 for the short-lived progeny ofradon (222Rn) and thoron (220Rn). The PAEC, cp, of any mixture of short-lived radon progeny
in air is the sum of the PAE of these atoms present per unit volume of air. Thus, if ci (in Bqm-3) is the activity concentration of decay product nuclide i, the PAEC of the progeny mixtureisc p = ∑ c i (ε p ,i λ r ,i )(Eq. 12-11)

i

8254
8255
8256
8257
8258
8259
8260

(614) The SI unit of this quantity is J m-3 (1 J m-3 = 6.242 1012 MeV m-3).
(615) The historical unit of PAEC that was used in the mining industry is the working
level (WL). A concentration of 1 WL is defined, in ICRP Publication 65 (ICRP, 1993), as
any combination of the short-lived radon progeny in 1 m3 of air that will result in theemission of 1.300 108 MeV of alpha energy (i.e. a PAEC of 1.300 108 MeV m-3).
(616) The so-called equilibrium equivalent concentration (EEC) is defined as the activity

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8261
8262
8263
8264

concentration of radon gas, in equilibrium with its short-lived progeny which would have thesame potential alpha energy concentration as the existing non-equilibrium mixture. It cantherefore be calculated as follows for a given radon progeny mixture:∑ c (ε λ )EEC =∑ (ε λ )
i

8265

p ,i

r ,i

i

p ,i

(Eq. 12-2)

r ,i

i

8266
8267
8268
8269
8270
8271
8272

(617) One WL equals approximately 3750 Bq m-3 of EEC of 222Rn (radon gas) orapproximately 275 Bq m-3 of EEC of 220Rn (thoron gas).
Table 12-2. Potential alpha energy per atom and per unit activity for radon (222Rn) and thoron(220Rn) progeny.
NuclideHalf-life
per atom
MeV

Radon (222Rn) progeny:
218
Po
3.05 min
13.69
214
Pb
26.8 min
7.69
214
Bi
19.9 min
7.69
214
Po
164 μs7.69
Total at equilibrium, per Bq of 222Rn
Thoron (220Rn) progeny:
216
Po
0.15 s14.6
212
Pb
10.64 h
7.8
212 a
Bi
60.6 min
7.8
212Po
304 ns8.78
220
Total at equilibrium, per Bq of Rn
8273
8274
8275
8276
8277
8278
8279
8280
8281
8282
8283
8284
8285
8286
8287
8288
8289
8290
8291

a 212

Potential alpha energy
per unit of activity
10-12 J
MeV Bq-1
10-10 J Bq-1
2.19
1.23
1.23
1.23

3.615 103
1.784 104
1.325 104
2 10-33.471 104

5.79
28.6
21.2
3 10-6
55.6

2.34
1.25
1.25
1.41

3.16
4.312 105
4.090 104
3.85 10-6
4.721 105

5.1 10-3
691
65.5
6.2 10-9756

Bi decays into 212Po and 208Tl with branching ratio of 64% and 36%.

Equilibrium factor, F(618) The equilibrium factor, F is defined as the ratio of the EEC to the radon gas
concentration. In other words, it is the ratio of the PAEC for the actual mixture of radon
decay products to that which would apply at radioactive equilibrium.
Exposure(619) The PAE exposure is defined as the time integral of the PAEC in air. The SI unit of
PAE exposure is J h m-3 and the historical unit applied to uranium mining is the working
level month (WLM). The WLM is defined as the cumulative exposure from breathing an
atmosphere at a concentration of 1 WL for a working month of 170 hours. The relationshipbetween the historical and SI units is as follows:
1 WLM = 3.54 mJ h m-3
1 mJ h m-3 = 0.282 WLM(620) One WLM equals approximately 6.37 105 Bq h m-3 of EEC of 222Rn (radon gas) orapproximately 4.68 104 Bq h m-3 of EEC of 220Rn (thoron gas). In terms of SI units, 1 J h m-3

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8294
8295
8296
8297
8298
8299
8300
8301
8302
8303
8304
8305
8306
8307
8308
8309
8310
8311
8312

equals approximately 1.80 108 Bq h m-3 of EEC of 222Rn gas or approximately 1.32 107 Bq h
m-3 of EEC of 220Rn gas. For 222Rn, if the exposure is expressed in terms of the radon gas
concentration then the two units are related via the equilibrium factor: 1 WLM = (6.37 105 /F) Bq h m-3 or 1 J h m-3 = (1.80 108 / F) Bq h m-3.
(621) Because of its short half-life, the gas activity concentration of thoron (220Rn) canvary substantially across an enclosed space and so it is not possible to use thoron gas
concentration in dose evaluation. Therefore, for control purposes, the PAEC of the thoron
progeny should be determined; that is, the EEC of thoron should be controlled. In ICRP
Publication 65 (ICRP, 1993), it was stated that ‘for protection against thoron, it is usually
sufficient to control the intake of the decay product, 212Pb, which has a half-life of 10.6
hours’. This is because the PAE per unit activity inhaled is about 10 times higher for 212Pb
than for other thoron progeny (Table 12-2). However, in this report doses are calculated for
exposures of thoron and its decay products, considering intakes of 212Pb as well as 212Bi and220
Rn.
Unattached fraction, fp(622) The unattached fraction, fp is defined as the fraction of the potential alpha energy
concentration (PAEC) of the short-lived progeny that is not attached to the ambient aerosol.
The magnitude of fp primarily depends on the concentration of particles of ambient aerosol, Z
and can be estimated with the semi-empirical equations given by Porstendörfer, (2001):
414
Z (cm −3 )150
fp =Z (cm −3 )8313

Radon (222Rn) progeny: f p =(Eq. 12-3)

8314

Thoron (220Rn) progeny:(Eq. 12-4)

8315
8316
8317
8318
8319
8320
8321
8322
8323
8324
8325
8326
8327
8328
8329
8330
8331
8332
8333
8334
8335
8336

(623) Porstendörfer and his colleagues measured the unattached fraction of radon andthoron progeny using a single screen diffusion battery with 50% penetration for 4 nm
diameter particles. A condensation nuclei counter was used to measure Z for particle
diameters > 5 nm. Equation (3) agrees fairly well with data for 2000 < Z < 7 105 cm-3
(Porstendörfer, 2001). At lower particle concentrations (Z< 400 cm-3), the agreement withdata is poor (Cheng et al., 1997). Also the above equation may underestimate fp in situations
where the radon progeny is far from equilibrium as is the case in some modern mines, which
are ventilated at a high rate to reduce radon concentrations (Cavallo et al., 1999). Because of
the relatively long radioactive half-life of the thoron decay product 212Pb (10 h), the fp value
for the thoron progeny is lower than that for the radon progeny under the same conditions.
Reasonable agreement was obtained between equation (4.4) and the data of Tschiersch et al.,2007, for 900 < Z < 3 104 cm-3.
Correlation between F and fp(624) For indoor air, F is weakly correlated with the unattached fraction, fp (Vaupotič,
2007; Vaupotič and Kobal, 2006, Marsh et al., 2002; Huet et al., 2001a; Vargas et al., 2000;
Chen et al., 1998; Tokonami, et al., 1996a; NRC, 1991; Vanmarcke, et al., 1989). This
negative correlation between F and fp has also been observed in a tourist cave (Vaupotič,
2008). The correlation can be explained as follows for conditions where the ventilation rate
is relatively low: When the aerosol particle concentration is high the unattached fraction islow, and the equilibrium factor is relatively high as more of the radon progeny are attached
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8338
8339
8340
8341
8342
8343
8344
8345
8346
8347
8348
8349
8350
8351
8352
8353
8354
8355
8356
8357
8358
8359
8360
8361
8362
8363
8364
8365
8366
8367
8368
8369
8370
8371
8372
8373
8374
8375
8376
8377
8378
8379
8380
8381
8382
8383

and stay in the air. More stay in the air because plate-out rates (i.e. deposition rates) for theaerosol attached nuclides are significantly lower than that for the unattached nuclides(Porstendörfer, 1994). Taking account of this negative correlation between F and fp, it has
been shown that for indoor air the radon gas concentration is a better index of dose than the
PAEC under a range of aerosol conditions normally encountered (Vargas et al., 2000; Marshand Birchall, 1998; Vanmarcke, et al., 1989; James et al., 1988). On this basis and because ofpractical considerations, radon gas measurements are generally carried out in homes andindoor workplaces. However, in mines with forced ventilation, the correlation between F and
fp is unlikely, so control of radon exposure in mines should be in terms of PAE exposure.
12.3.

External dose(625) Radon progeny in the ambient air can plate-out (i.e. deposit) on surfaces including
human skin. The alpha particles emitted will deliver a dose to the outer layers of the skin inareas exposed to the atmosphere such as neck and face whereas skin protected by clothing andhair will in general receive a minimal dose (AGIR, 2009). The amount of radon progeny
depositing on the skin for a given air concentration mainly depends on the deposition
velocity, which in turn depends on particle size and air movement. The BEIR VI report(NRC, 1999) gives values of absorbed dose rate to exposed areas of the skin as a result ofdomestic exposure to 222Rn based on the work of Harley and Robbins (1992) and of Eatoughand Henshaw (1992). The latter authors give estimates of equivalent dose to skin of 1.4 10-8
Sv per Bq h m-3 (range 0.97 10-8 to 9.710-8 Sv per Bq h m-3 ) for 222Rn and 1.1 10-7 Sv per Bq
h m-3 (range 0 to 7.2 10-7 Sv per Bq h m-3) for EEC of 220Rn. These values relate to thebasal cell layer of the face and neck with an assumed epidermal thickness of 50 μm. The
values for 222Rn were calculated assuming F= 0.5 (and fp =0.03), so the estimated equivalentdose to skin in terms of mSv per WLM for indoor exposure is about 18 mSv per WLM(range 12 to 124 mSv per WLM). The estimated range mainly reflects the uncertainties in thedeposition velocity of the radon progeny. As the tissue weighting factor for the skin is 0.01,
this skin dose contributes a small amount to the overall effective dose (Table 12-15).
(626) Charles (2004), point out that currently there is no definitive answer to the locationand the identity of the target cells in the skin that play a dominate role in the induction of skincancer. It has generally been assumed by several authors that the basal cell layer of theepidermis is the target cell layer. However, there are existing animal data that imply that thetarget cells are in the underlying dermis, in which case they may lie too deep to receive any
significant dose from radon progeny on skin surface. In this report, the calculation ofeffective dose from exposure to radon and its progeny does not include dose to skin fromradon progeny deposited on skin surface.
(627) The external dose from submersion in a cloud of radon and its decay products is notconsidered in this report.
12.4.

Routes of Intake

12.4.1. Inhalation(628) Consideration is given to the two components of exposure:• Inhalation of the short-lived decay products;• Inhalation of radon gas.

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
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8386
8387
8388
8389
8390
8391
8392
8393
8394
8395

(629) Absorption parameter values for radon decay products are addressed in theinhalation sections of the elements (lead, bismuth and polonium) and are given in Table 12-3.
As described in OIR part 1, Section 3.2.3 shared kinetics are assumed in the respiratory tract.
However, analysis has shown that the application of independent kinetics in the respiratory
tract rather than shared kinetics would make little difference to the lung dose; less than about5%.
(630) Information is available on the behaviour of inhaled radon and other inert gases inman. This information is given in Section 12.4.3, which describes the biokinetic model forradon following inhalation and ingestion.
Table 12-3. Absorption parameter values for inhaled radon progeny
Inhaled radon progeny

Polonium
Lead
Bismuth
8396
8397
8398
8399
8400
8401
8402
8403
8404
8405
8406
8407
8408
8409
8410
8411
8412
8413
8414
8415
8416
8417
8418
8419
8420
8421
8422
8423
8424

Dissolution
valuesfr
1
0.1
1

sr (d–1)
3
100
1parameter Uptake
valuesss (d–1)
–
1.7
–

fb
–
0.5
–

parameter Absorption
fromthealimentarySb (d–1)
tract, fA
–
0.1
1.7
0.02
–
0.05

Inhalation of the short-lived decay products of 222Rn(631) Aerosol characteristics need to be defined in order to calculate doses from inhalingradon progeny. The activity size distribution of the radon progeny aerosol can be veryvariable and depends upon the exposure scenario. For the purposes of dose calculation,
aerosol parameter values are given for indoor workplaces and mines (Table 12-4). However,for completeness measured values of aerosol parameters for tourist caves, water supply
facilities and thermal spas are also discussed. Because the absolute risk of lung cancer frominhaling radon and its progeny is greatly influenced by tobacco smoking, choosing aerosolparameter values other than those given in Table 12-4 is considered generally not to be
warranted for radiation protection purposes.
(632) The relative activity size distribution of unattached radon progeny clusters depends
on the concentration of water vapour, trace gases and the electrical charge distribution of theradionuclides in the air. Porstendörfer (2001) found that under ‘normal’ conditions ofhumidity and radon concentration, the activity size distribution of the unattached progeny canbe approximated with three lognormal distributions. The AMTD values measured were 0.6
nm, 0.85 nm, and 1.3 nm with geometric standard deviations (σg) of about 1.2. In places withhigh radon concentrations, the fraction with the greatest AMTD value (1.3 nm) was notobserved.
The neutralisation rate of the unattached clusters increases with radon
concentration and so it is likely that modes below 1 nm are mainly associated with neutralclusters, whereas modes above 1 nm are charged clusters (Porstendörfer et al., 2005). Huet etal. (2001b) also measured the size distribution for the unattached radon progeny and found a
unimodal distribution with median diameters between 0.5 and 1.5 nm and values of σg
between 1.2 and 1.4. Other workers have also measured a unimodal distribution in the range
0.7 – 1.7 nm (Cheng et al., 1997; El-Hussein, et al., 1998; Mohammed, 1999; El-Hussein,2005). For the purposes of dose calculation and for simplicity, a unimodal distribution withan AMTD of 0.9 nm and a σg of 1.3 is assumed here for all exposure scenarios.
(633) The size of the unattached radon progeny is assumed to remain constant in the lung
(NRC, 1991). However, some of the ambient aerosols, to which radon progeny attach, are

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8426
8427
8428
8429
8430
8431
8432
8433
8434
8435
8436
8437
8438
8439
8440
8441
8442
8443
8444
8445

unstable in saturated air (i.e. hygroscopic) and are assumed to grow very quickly on inhalation
by a given factor (Sinclair et al., 1974; NRC, 1991). For modelling purposes and simplicity, it
is assumed that the AMTD increases by the hygroscopic growth factor (hgf) instantaneously
as the particle enters the nose or mouth. Assumed values for the hgf are given in Table 12-4
for different exposure scenarios.
(634) Porstendörfer (1996) pointed out that results of experimental studies show that thedifferences between the activity size distribution of the individual decay products attached on
aerosol particles are negligible. Therefore, for simplicity and for dosimetry purposes, theaerosol distribution of each of the short-lived 222Rn progeny (i.e. of 218Po, 214Pb and 214Bi) is
assumed to be the same.
(635) Low pressure cascade impactors, which measure the aerodynamic diameter, can beused to measure the activity size distribution of the attached progeny. Such results are
expressed in terms of an AMAD with a σg for a given mode of the attached size distribution(Reineking et al., 1994). However, measurements carried out with diffusion batteries measure
the thermodynamic diameter and the results are expressed in terms of AMTD with a σg for agiven mode. For particle sizes less than 500 nm diffusion is the dominate mechanism ofdeposition in the respiratory tract and the AMTD is the parameter that characterises
deposition by diffusion.

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DRAFT REPORT FOR CONSULTATION: DO NOT REFERENCE
8446
8447
8448
8449
8450

Table 12-4. Aerosol parameter values for different exposure scenarios for 222Rn progeny
Exposure scenario

8451
8452
8453
8454
8455
8456
8457
8458

fp a, b

Equilibrium
factor, F

Indoor workplace

0.1

0.4

Mine

0.01

0.2

Attached aerosol characteristics in the ambient airc
Mode, i
fpi
AMADi
Density, ρi(nm)(g cm-3)
n
0.2
30
1.4
a
0.8
250
1.4
a
1.0
0.7e

a

Shape factor,
χi
1.1
1.1
1.0e

AMTDi
(nm)
24
213
250

σgi

hgfid

2.0
2.0
2.0

2.0
2.0
1.0

fp = unattached fraction in terms of the potential alpha energy concentration (PAEC).
The unattached progeny are assumed to have an AMTD of 0.9 nm with σg = 1.3, and unit density and shape factor.
cIndices i = n and a represent the accumulation and nucleation modes. fpi = fraction of attached PAEC for mode i. σgi = geometric standard deviation of mode i. hgfi =hygroscopic growth factor for mode i.
d
It is assumed that the AMTD increases by hgf instantaneously as the particle enters the nose or the mouth. For simplicity, the hygroscopically enlarged particles are assumed
to have unit density and shape factor.
e
The values chosen for the density (ρ) and shape factor (χ) for a diesel powered mine aerosol are based on the measurements of the effective density, (i.e. ρ/χ) of diesel
exhaust particles and is assumed to be ρ/χ = 0.7 g cm-3 (Park et al., 2003; Olfert et al., 2007).
b

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8460
8461
8462
8463
8464
8465
8466
8467
8468
8469
8470
8471
8472
8473
8474
8475
8476
8477
8478
8479
8480
8481
8482
8483
8484
8485
8486
8487
8488
8489
8490
8491
8492
8493
8494
8495
8496
8497
8498
8499
8500
8501
8502
8503
8504
8505

Indoor workplaces(636) Published data on activity size distributions in indoor workplaces other than homes
are relatively sparse. Reichelt et al. (2000) carried out activity size measurements of radon
progeny at several workplaces including offices, workshops, factories, kitchens, agricultural
facilities and public buildings like schools, hospitals and art galleries. Porstendörfer (2001)
summarised their results and suggested dividing indoor workplaces into two categories:
workplaces in rooms without coarse particles, and workplaces with coarse particles generated
by human activities and dispersion processes. Calculated values of the equivalent dose to thelung per unit exposure for the two categories differed by less than 10% (Porstendörfer, 2001).
In this report workplaces in rooms without coarse particles are considered.
(637) The parameter values of the activity size distribution for the attached radon progeny
assumed for indoor workplaces (Table 12-4) are based primarily on the measurement resultsof Porstendörfer (2001) and on results published for homes. Marsh et al. (2002) summarises
measurement results for homes published in the literature since 1980.
(638) For an aged aerosol (i.e. without additional aerosols), the presence of a nucleation
mode is not always measured but can be observed when additional aerosols are produced(Marsh et al., 2002; Huet et al., 2001b; Tu et al., 1991; NRC, 1991). For an aged aerosol,
Huet et al. (2001b) found that the attached size distribution consisted only of theaccumulation mode. However, intercomparison measurements performed in a house inGermany, without additional aerosols, showed nucleation and accumulation modes with thefraction of the attached PAEC in the nucleation mode (fpn) being about 0.2 (Reineking et al.,1994). Measurements of the activity size distribution of the attached progeny in a dwelling in
Okinawa, Japan also showed a nucleation mode with an activity fraction of 0.14 (Kranrod etal., 2009). The mean AMAD of the nucleation mode was about 30 nm with a σg of 1.6.
Porstendörfer (2001) reported values of fpn between 0.2 and 0.5 for workplaces. The AMADof the nucleation mode was reported to be between 15 to 40 nm with a σg ranging between
1.6 and 2.2. A fpn value of 0.2 is assumed here for indoor workplaces. An AMAD of 30 nmwith a σg of 2.0 is assumed for the nucleation mode.
(639) Indoor measurements of the AMAD of the accumulation mode show a wide range ofvalues, typically between 110 – 370 nm (Huet et al., 2001b, Porstendörfer, 2001, Mohammed,
1999, El-Hussein et al., 1998; Tu et al., 1991; Tu and Knutson, 1988). A central value of 250
nm is assumed here with a σg of 2.0.
(640) Sinclair et al. (1974) found that atmospheric particles in their laboratory increased indiameter by about a factor of 2 when the relative humidity increased from zero to 98%. For
indoor workplaces a hygroscopic growth factor (hgf) of 2.0 is assumed here for the ambient
aerosol. The density (g cm-3) and the shape factor of these hygroscopically enlarged particles
are taken to be unity.
(641) Measurements of the unattached fraction, fp, in indoor workplaces such as schools
and offices show a wide range of values, typical between 3% and 15% and with some values
greater than 20% (Vaupotič, 2008b; Porstendörfer, 2001; Yu et al., 1998; Tokonami et al.,1996b; Hattori et al., 1995, Hattori and Ishida, 1994). Typical values of fp in homes range
between 4% and 20% with some values greater than 40% (Kranrod et al., 2009; El-Hussein,
2005; Mohamed, 2005; Vargas, et al., 2000; Tokonami, et al., 1996a; Yu, et al., 1996; Hopke,
et al., 1995; Reineking and Porstendörfer, 1990; Chen, et al., 1988; Kojima and Abe, 1988).
A representative value of fp = 0.1 is chosen for indoor workplaces.
(642) The value of the equilibrium factor, F, depends mainly on the indoor ventilation rate
due to opening/shutting of windows, use of electric fans, air conditioners and dehumidifiers.

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8509
8510
8511
8512
8513
8514
8515
8516
8517
8518
8519
8520
8521
8522
8523
8524
8525
8526
8527
8528
8529
8530
8531
8532
8533
8534
8535
8536
8537
8538
8539
8540
8541
8542
8543
8544
8545
8546
8547
8548
8549
8550
8551
8552
8553

(Iyogi et al., 2003; Iimoto, 2000; Iimoto et al., 2001; Chen, et al., 1998). Typically, meanvalues of F ranged from 0.3 to 0.6 for schools, kindergardens, offices, nuclear power plant,
factories and cafes (Labidi et al., 2010; Vaupotič, 2008b, Maged, 2006; Misdaq and Amghar,
2005; Iyogi et al., 2003; Misdaq and Flata, 2003; Tokonami et al., 2003, 1996; Yu et al.,2000, 1998; Hattori et al., 1995; Hattori and Ishida, 1994). In its 2000 report, UNSCEAR
assumed an F value of 0.4 for indoor exposures, based mainly on measurements in dwellingsin the USA (Hopke et al., 1995) and in India (Ramachandran and Subba Ramu, 1994). A F
value of 0.4 is assumed here for indoor workplaces, which is in agreement with the value
given in ICRP Publication 65 (ICRP, 1993).
Mines(643) Characterising the aerosol parameters for mines is difficult because of the highlyvariable conditions and because of the different types of mining conditions such as use ofdiesel or electric powered equipment, different ventilation rates, and the type of heating usedduring the winter months (Marsh et al., 2008; Cavallo, 2000).
(644) Measurements were made of the activity size distribution in two mines in the USA in
Colorado and New Mexico (Cooper et al., 1973). Because the measurements were madeduring wintertime, it is likely that the incoming ventilation air was heated by burning propane
gas. However, it is not clear from the report whether the heaters were being used when themeasurements were made. Both mines used diesel engines. The measurements were carriedout with a low pressure impactor having five stages and a backup filter. However, its
resolution was relatively poor. These data were reanalysed by Cavallo (1998) using modern
unfolding techniques. The reanalysed data showed that for the Colorado mine the AMAD ofthe principal mode ranged from 111 nm to 303 nm with a mean of 200 nm. The mean valueof σg was 2.0. Four out of the nine spectra had a secondary mode with a peak around 30 nm
containing about 20-25% of the PAEC. However, given the poor resolution of the impactor
the authors did not consider this secondary mode in their dose calculations. For the New
Mexico mine, the mean values of the AMAD and σg of the accumulation modes were 140 nm
and 2.9 respectively (Cavallo, 1998).
(645) Measurements were carried out in four uranium mines in New Mexico, USA during
the summer of 1971 (George et al., 1975). All four mines were diesel powered with one of
the mines being much less active than the others. The activity size measurements obtainedwith a diffusion battery were reanalysed by Knutson and George (1990). Twenty six spectra
were obtained; nine of the spectra were unimodal with a mean AMTD of 150 nm ( 80 – 210nm) and a σg of about 2.7, and 11 spectra had both unattached and accumulation modes. The
remaining six spectra showed one activity peak at 100 – 200 nm and another at 5 – 10 nm.
The average value of the equilibrium factor was 0.17.
(646) During the summer of 1978 measurements were carried out with a diffusion battery
in a Canadian diesel powered uranium mine (Busgin et al., 1981). An AMTD of about 100
nm with a σg of 1.9 was measured in an exhaust ventilation area of the mine. The unattachedfraction of 218Po was estimated to be less than 2%. Based on the measured particle
concentration (105 cm-3), fp is calculated to be about 0.4%. The same group also carried out asecond set of measurements during the winter of 1985 in two mines in Canada; one mine useddiesel equipment and the other used electrically powered equipment (Kahn et al., 1987). In
the diesel powered mine the AMTD was about 90 nm with a σg of 1.8 whereas in theelectrically powered mine the AMTD was about 50 nm with a σg of 1.8. The measurements
were carried out with a set of diffusion batteries which had relatively poor resolution.
(647) Activity size measurements have been performed at a diesel powered uranium mine
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8555
8556
8557
8558
8559
8560
8561
8562
8563
8564
8565
8566
8567
8568
8569
8570
8571
8572
8573
8574
8575
8576
8577
8578
8579
8580
8581
8582
8583
8584
8585
8586
8587
8588
8589
8590
8591
8592
8593
8594
8595
8596
8597
8598
8599
8600
8601

in France, at the Bellezane mining centre during the summer of 1989 (Boulaud and Chouard,
1992). The gallery cross section was 10 m2 with mean air velocities of about 1 m s-1. A
combination of a cascade impactor in series with a diffusion battery was used to carry out themeasurements. The AMTD ranged from 150 nm to 210 nm with a mean of 178 nm. The
aerosol concentration was also measured; mean values per half day varied from 6 104 to 9 104
cm-3. This indicates fp values of less than about 1%.
(648) Butterweck et al. (1992) carried out activity size measurements in undergroundmines in Germany with a low pressure cascade impactor and a high volume impactor. The
unattached fraction was also measured with wire screens. Their results showed that withdiesel engines, the diesel aerosol dominates the mine aerosol resulting in a very low
unattached fraction; 0.1% - 2.5% with a mean of 0.7%. In the diesel powered slate mine, theyfound that during working hours the AMAD of the accumulation mode was about 200 nm
with a σg of about 2.0. During non-working hours the AMAD increased to about 350 nm.
For the other active mines in Germany (barite: Dreislar, Bad Lauterberge; iron: Salzgitter;uranium: Groβ-Schloppen), the mean values of the AMAD ranged from 180 – 270 nm during
working hours. The equilibrium factor value ranged from 0.3 to 0.6 with a mean of 0.45.
(649) Solomon et al. (1993, 1994) carried out activity size distributions measurements inan underground uranium mine, at Olympic Dam, South Australia. Measurements werecarried out with a serial graded screen array and a diffusion battery. In areas of the mine
where there were large diesel-powered vehicles, the AMTD of the accumulation mode ranged
from 200 to 300 nm. The average value of the AMTD was 250 nm with a σg of about 2.5. In
the areas of the mine where there were no vehicles or the ventilation intakes were close by,
the AMTD values were smaller in the range 90-200 nm with a mean of 150 nm. The meanvalue of the unattached fraction throughout the mine was about 3% to 4% and the mean valueof the equilibrium factor was about 0.2.
(650) Measurements have been carried out to characterise the aerosol in a wet undergrounduranium mine in northern Saskatchewan, Canada (Cavallo, 1997, 2000; Cavallo et al., 1999,
Wu-Tu et al., 1997). This mine used state-of-the art mining technology and used diesel
powered equipment extensively. Because of the exceptionally high grade ore, the mine
ventilation rate was very high; about 3.6 104 m3 min-1, which was estimated to be about one
air change per 3 minutes. The average air velocity in the main decline was about 5 m s-1 (12mph). Measurements were carried out in the winter of 1995 and in the summer of 1996. An
impactor with a graded screen array was used to determine the size distribution over a rangeof particle sizes of 0.6 to 5000 nm. During the winter months the temperature inside the mine
was maintained at 5ºC by direct burning of propane gas to heat the ventilation air. As aresult, the mine aerosol consisted of particles from the combustion of propane gas as well as
diesel particles. The winter time measurements carried out at a stope and a drilling area whereminers were working showed predominately a two modal distribution for the attachedprogeny. The fraction of the attached PAEC associated with the nucleation and accumulation
modes were about 65%, and 35%, and the mean values of the AMAD were about 60 nm and
330 nm respectively. The unattached fraction (fp) was about 1%. Winter time measurements
were also carried out at a bolt-storage bay next to a major mine exhaust. Most of thesemeasurements showed that the attached progeny consisted of the nucleation mode containing
about 97% of the attached PAEC, on average, with AMAD values between 50 and 75 nm.
The coarse mode accounted for the remaining 3% of attached PAEC with an AMAD between
2 and 8 μm. Typically fp was less than 2% and the mean value of the AMTD of theunattached progeny was less than 1 nm. The results of the summer time measurements of1996 showed that throughout the mine the AMAD values ranged from 50 nm to 120 nm with216

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
8602
8603
8604
8605
8606
8607
8608
8609
8610
8611
8612
8613
8614
8615
8616
8617
8618
8619
8620
8621
8622
8623
8624
8625
8626
8627
8628
8629
8630
8631
8632
8633
8634
8635
8636
8637
8638
8639
8640
8641
8642
8643
8644
8645
8646
8647
8648
8649

a mean value of 85 nm and σg of about 2.0. The average value of fp was about 6% whereas
the expected value based on particle concentration was 0.3%. This unexpected high value offp was theoretically shown to occur under conditions when the radon progeny is far fromequilibrium as was the case in this Canadian mine, which was ventilated at a high rate
(Cavallo et al., 1999). The average value of the equilibrium factor was 0.08.
(651) Tokonami, et al. (2005) measured the activity size distribution in an undergroundmine located in the Gifu prefecture region of Japan. A cascade impactor with ten stages and a
graded screen array were used for the measurements. The AMTD of the unattached progeny
was 0.8 nm with a σg of 1.5. The activity size distribution of the attached progeny was
represented by a single mode having an AMAD of 162 nm with a σg of 3.1.
(652) Based on the measurements of Cooper et al. (1973) in US mines and themeasurements of Bigu and Kirk (1980) in Canadian mines, a panel of experts from the
National Research Council (NRC, 1991) recommended an AMTD of 250 nm in areas ofactive mining and a fp value of 0.5%. In areas of transport and maintenance work (i.e.
haulage drifts), a fp value of 3% was assumed. In these areas a lower AMTD value of 150 nm
was assumed based on the measurement data of George et al., 1975, which was reanalysed byKnutson and George (1990).
(653) Aerosol parameter values are given for a diesel powered mine with medium to good
ventilation (Table 12-4). These chosen values are mainly based on the measurements carriedout in mines in Australia (Solomon et al., 1993, 1994), France (Bouland and Chouland, 1992)
and Germany (Butterweck et al., 1992). For diesel powered mines it is assumed that theaerosol does not increase in size in the respiratory tract because diesel aerosols arehydrophobic (Cavallo, 2000; Weingartner et al., 1997).
(654) For a diesel powered mine it is assumed that the aerosol is mainly dominated by the
diesel aerosol. Several workers have calculated the effective density of diesel exhaust
particles from measurements of the thermodynamic diameter (dth) and aerodynamic diameter(dae) of the exhaust particles (Park et al., 2003; Olfert et al., 2007). The effective density is
the ratio of the particle density (ρ) and shape factor (χ). Results indicate that the effective
density decreases with increasing dth in the size range from 50 – 300 nm. This mainly occurs
because particles become more highly agglomerated as size increases. The smaller particles
are more compact than the larger particles and therefore have a higher effective density.
Typically, the effective density varies from 1.2 to about 0.3 g cm-3 depending on size and fuelcomposition; higher effective densities are observed for high sulphur fuel. The chosen values
for the effective density of the aerosol in diesel powered mines are based on themeasurements of Park et al. (2003) and Olfert et al. (2007).
(655) It is acknowledged that the exposure conditions in mines today are significantly
different from those 10 to 20 years ago and that the chosen aerosol parameter values are notnecessarily representative of mines today. However, there are currently no published data on
aerosol characteristics in modern mines.
Tourist caves(656) Information on exposure conditions in tourist caves is given here for completeness.
Reference parameter values for tourist caves are not given in this report.
(657) Typically there is no additional ventilation in tourist caves as forced ventilation may
alter the humidity inside the cave affecting some of the geological formations that attract
tourists. As a result radon concentrations can reach high levels of several thousand Bq m-3(Butterweck et al., 1992; Sainz et al., 2007). Several measurements have been carried out innatural caves to characterise the aerosols.
217

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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8651
8652
8653
8654
8655
8656
8657
8658
8659
8660
8661
8662
8663
8664
8665
8666
8667
8668
8669
8670
8671
8672
8673
8674
8675
8676
8677
8678
8679
8680
8681
8682
8683
8684
8685
8686
8687
8688
8689
8690
8691
8692
8693
8694
8695
8696
8697

(658) Butterweck et al. (1992) carried out activity size measurements in a natural tourist
cave, in Postojna, Slovenia, with a low pressure cascade impactor and a high volume
impactor. The unattached fraction was also determined from wire screen measurements. The
AMAD of the accumulation mode ranged from 120 nm to 290 nm with a mean of 230 nm.
The mean σg value of the accumulation mode was 2.2. The fp value varied from 6% to 16%
with a mean of 10%. The average value of the particle concentration was about 3000 cm-3.
The F value range from about 0.3 to 0.5 with a mean of 0.4.
(659) Solomon, et al. (1992) used a parallel wire screen diffusion battery and a serial
graded screen array battery to measure the activity size distribution of the radon progeny in alimestone cave, Victoria, Australia. Measurements were carried out over a 3 day period
during October 1990 at different sites in the cave. The accumulation mode had an AMTD of
170 nm and the unattached mode had an AMTD of 1.1 nm. The fp value throughout the cavevaried from 11% to 18% whereas the F factor varied from 0.2 to 0.5. The average fp value
weighted by the occupancy of the tour guides in each sampling site was 14%. Measurementsof the radon concentration carried out during June and October indicated that the radon
concentration is relatively constant throughout the year.
(660) Measurements have been carried out over a 3 day period during the summer of 1994
in the Carlsbad Caverns, in southern New Mexico to determine air exchange rate, aerosol
characteristics and radon progeny activity size distributions (Cheng et al., 1997). During thesummer months the outside air temperature is much greater than inside the cave, which keeps
the cave air stagnant. The mean ventilation rate was measured to be 2 10-3 h-1, which wasestimated to be one air exchange every 18 days. The measured particle concentration wasvery low; average daily values were between 280 and 385 cm-3. As a result the measured fp
values were high; values ranged from 25% to 60% with a mean of 44%. The average value of
F was 0.4. The activity size measurements were carried out with a graded diffusion battery.
The AMTD of the unattached particles were between 0.6 and 0.8 nm, and the attached mode
had a peak > 50 nm. It was noted that the particle concentration measurements made in thesame area of the cave during summer months by Wilkening and Romero (1981) were morethan twice as high, indicating fp values lower by a factor of 2 or more.
(661) Sainz et al. (2007) carried out radon concentration and particle concentration
measurements in tourist caves located in the region of Cantabria in the North of Spain. The
results of the particle concentration measurements were 464 cm-3 in the Castillo cave and1514 cm-3 in the Monedas cave. This indicates fp values of 86% and 26% respectively.
(662) Measurements of the unattached fraction and equilibrium factor have been carriedout in the Postojna Cave, Slovenia for 10-15 days during summer and winter months ofconsecutive years from 1998 to 2001 (Vaupotič, 2008a). Measurements were carried out at
the railway station in the cave and at the lowest point of a walking tour. There is no forced
ventilation in the cave; however during the winter months there is a natural draught of air
from the cave to the outdoors as the temperature in the cave is greater than the outdoor
temperature, whereas in the summer months this draught is minimal. As a consequence, theradon concentration in the cave is higher in the summer compared with the winter. The
measurement results show that unattached fraction is higher in the summer compared with thewinter. At the lowest point of the cave, mean values of fp were about 60% in the summer andabout 12% in the winter; the mean values of F were about 0.3 in the summer and 0.6 in thewinter. Values of F were negatively correlated with fp. At the railway station during thesummer, mean values of fp and F were 17% and 0.6 respectively.
(663) Rosvenská, et al. (2008) measured the unattached fraction, equilibrium factor and theparticle size spectrum in the Bozkov dolomite cave, Czech Republic. The fp value was low
218

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8698
8699
8700
8701
8702
8703
8704
8705
8706
8707
8708
8709
8710
8711
8712
8713
8714
8715
8716
8717
8718
8719
8720
8721
8722
8723
8724
8725
8726
8727
8728
8729
8730
8731
8732
8733
8734
8735
8736
8737
8738
8739
8740
8741
8742
8743
8744
8745

and varied between 1% and 3%. The F value was about 0.7. The activity size distribution
was theoretically determined from the particle size distribution. For the attached progeny the
AMAD and σg of three modes were calculated: 140 nm with σg = 1.7; 720 nm with σg = 1.4
and 1.9 μm with σg = 1.9. The fraction of the PAEC associated with each mode was not
given.
Water Supply facilities and Spas
(664) Information on exposure conditions in water supply facilities and spas is given here
for completeness. Reference parameter values for water supply facilities and spas are notgiven in this report.
(665) High levels of 222Rn gas concentrations in indoor air have been measure at watersupply facilities where ground water with a high radon concentration is treated or stored(Trautmannsheimer, 2003). Porstendörfer and Reineking (1999) measured the activity size
distribution at a water supply station in Germany. About 84% of the attached PAEC wasassociated with the accumulation mode, having an AMAD of 300 nm with a σg=1.8. The
remaining 16% of the attached PAEC was associated with the nucleation mode, having an
AMAD of 50 nm with a σg=1.5. They reported a fp value of 0.05. The relative humidity at awater supply station was reported to be close to 100% (Porstendörfer, 2001).
(666) Thermal spa facilities have been used for medical therapy and rehabilitation centres
as well as for recreational purposes. Radon emanating from the thermal waters is anadditional source of radiation exposure to the working personnel as well as to the bathers.
Measurements of 222Rn in air in thermal spas have shown that the dominant mechanism bywhich 222Rn is released from water to air is during bath filling and to a lesser extent duringbathing as a result of water agitation (Vogiannis et al., 2004a, Lettner et al., 1996). Duringbathtub filling, F is initially low but then gradually increases and reaches a peak with a timedelay preceding a 222Rn peak.
Correspondingly, the fp value is initially high but thendecreases and reaches a minimum. Average values of F and fp have been reported formeasurements carried out in treatment/bath rooms, rest rooms and reception rooms of spas in
Greece (Vogiannis et al., 2004b, 2004c); average values of fp range from 0.06 to 0.12 and F
values range from 0.2 to 0.4. However, Geranios et al. (2004) reported higher values of fp ofabout 0.23 in a treatment room and a reception room of the spa of Loutra Eipsou, Greece.
Values of F measured in treatment rooms of spas in Slovenia and Austria range from 0.14 –0.45 (Vaupotič and Kobal , 2001; Lettner et al., 1996). In two Spanish spas, the estimatedaverage F value was 0.6 (Soto and Gómez, 1999).
Inhalation of the short-lived decay products of 220Rn(667) Thoron (220Rn) decays into the short-lived progeny of 216Po, 212Pb, and 212Bi (Figure
12-2, Table 12-2. As can be seen from Table 12-2, the PAE per unit activity of 212Pb is about
10 times higher than for other thoron progeny. As a consequence, ICRP Publication 65(ICRP, 1993) states that “For protection against thoron, it is usually sufficient to control the
intake of the decay product, lead-212, which has a half-life of 10.6 hours.” In this report the
intake of 212Bi is also considered, but most of the dose arises from the intake of 212Pb. The
activity size distribution of 212Bi attached on aerosols is assumed to be the same as that for
212
Pb.
(668) Published data on the activity size distributions of the thoron decay product, 212Pb
are relatively sparse. It has been suggested that because of the longer radioactive half-life of212
Pb compared with that of 222Rn progeny that the aerosol size of attached 212Pb is likely to
be larger compared with that of 222Rn progeny (Khan et al., 1987). The longer half-life means
219

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8747
8748
8749
8750
8751
8752
8753
8754
8755
8756
8757
8758
8759
8760
8761
8762

8763
8764
8765
8766
8767
8768
8769
8770
8771
8772
8773
8774
8775
8776
8777
8778
8779
8780
8781
8782
8783
8784
8785
8786
8787

that atoms of 212Pb can spend more time in the vicinity of aerosols leading to increased
coagulation of aerosols and larger particle sizes. However, measurements show that themedian diameters of the accumulation mode for 212Pb and the radon decay product, 214Pb are
similar at least for ‘typical’ indoor air (Becker et al., 1984; Reineking et al., 1992). For the
purposes of dose calculation, aerosol parameter values for thoron progeny are given in Table
12-5 for indoor workplaces and mines.
(669) The size distribution of the unattached thoron progeny is assumed to be the same asthat for 222Rn progeny. A unimodal lognormal distribution with an AMTD of 0.9 nm with a
σg of 1.3 is assumed for all exposure scenarios. This is in agreement with what is measured
for indoor and mining environments, where the unattached 212Pb was found to have particle
sizes around 1 nm (Chen, et al., 1997). Measurements carried out in a radon test chamber, as
part of an intercomparison exercise, also showed medium diameters less than 1 nm forunattached 212Pb (Cheng, et al., 2000).
Table 12-5. Aerosol parameter values for different exposure scenarios for thoron (220Rn)progeny.
Exposure
scenario

fp a, bIndoorworkplace

0.02

Mine

0.005

Attached aerosol characteristics in the ambient airc
Mode, i fpi
AMADi Density,ρi
Shape
AMTDi σgi
(nm)
(g cm-3)factor, χi (nm)
n
0.14
40
1.4
1.1
32
2.0
a
0.86
200
1.4
1.1
170
1.8
a

1.0

0.7

1.0

250

2.0

hgfid
2.0
2.0
1.0

a

fp = unattached fraction in terms of the potential alpha energy concentration (PAEC).
b
The unattached progeny are assumed to have an AMTD of 0.9 nm with σg = 1.3, and unit density and shapefactor.
c
Indices i = n and a represent the accumulation and nucleation modes. fpi = fraction of attached PAEC for modei. σgi = geometric standard deviation of mode i. hgfi = hygroscopic growth factor for mode i.
d
It is assumed that the AMTD increases by hgf instantaneously as the particle enters the nose or the mouth. For
simplicity, the hygroscopically enlarged particles are assumed to have unit density and shape factor.

Indoor air(670) Becker et al. (1984), measured the activity size distribution of 212Pb in different
buildings in the city of Göttingen, and in the countryside of Germany. Measurements werecarried out with a high volume cascade impactor. The size distribution of the attachedaerosol could be approximated by a log-normal distribution. Values of AMAD ranged from
120 nm to 290 nm with a mean of 200 nm. The mean value of σg was 2.9. The mean valueof the AMAD for the city results was similar to that of the countryside results but the σg forthe countryside results was larger.
(671) Reineking et al. (1992) measured the activity size distribution of 212Pb in sevenrooms of different houses in Germany. Measurements were performed with a low pressure
cascade impactor. For separating unattached from aerosol-associated thoron progeny, a single
screen with a 50% penetration for 4 nm diameter particles was used. The AMAD of theaccumulation mode was about 200 nm with a σg of 1.8. Between 6% and 20% of the attachedactivity was associated with the nucleation mode with a mean of 14%. The nucleation mode
had an AMAD less than 80 nm. These results were also reported by Porstendörfer (2001).
Porstendörfer reports that the nucleation mode has an AMAD between 30 to 50 nm with a σgof about 2. Porstendörfer noted that the fraction of the attached 212Pb activity associated with220

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
8788
8789
8790
8791
8792
8793
8794
8795
8796
8797
8798
8799
8800
8801
8802
8803
8804
8805
8806
8807
8808
8809
8810
8811
8812
8813
8814
8815
8816
8817
8818
8819
8820
8821
8822
8823
8824
8825
8826
8827
8828
8829
8830
8831
8832
8833
8834
8835

the nucleation mode is lower than the corresponding values for radon (222Rn) progeny. The
unattached fraction (fp) of thoron progeny for ‘typical’ indoor air with aerosol particle
concentration of (5-15) × 103 cm-3 is between 0.01 and 0.03.
(672) Zhang et al. (2010) measured activity size distributions of 212Pb in countryside andcity dwellings of China. There were no appreciable differences among the particle size
distribution from dwellings within the same area and under the same climate conditions.
However, the particle size distribution measured in countryside dwellings were lower than incity dwellings. In city dwellings of Beijing, the AMAD of 212Pb was about 150 nm with a σgof 2.0 and in the suburbs of Beijing the AMAD was about 110 nm with a σg of 2.0. For someof the countryside dwellings of Yangjiang, Guuangdong Province, which were mainly madeof brick, the mean AMAD was 80 nm with a σg of 2.9. For the cave dwellings of Datong,
Shanxi Province, the mean AMAD was 50 nm with a σg of 3.1.
(673) The aerosol parameter values assumed for thoron progeny for indoor workplaces are
based on the measurements of Reineking et al., 1992 and on the values recommended by
Porstendörfer, 2001 (Table 12-5).
Mine(674) The activity size distribution of 212Pb was measured with a diffusion battery in a
Canadian diesel powered uranium mine during the summer of 1978 (Busgin et al., 1981).
Measurements were carried out in an exhaust ventilation area of the mine where there was nowork of any kind in progress. The average value of the AMTD was found to be about 90 nm
with a σg from 1.5 to 2.3. The same group also carried out a second set of measurements
during the winter of 1985 in a diesel powered mine and in an electrical powered mine (Kahn
et al., 1987). The mean AMTD of 212Pb was about 100 nm with a σg of 1.7 in the diesel
powered mine whereas in the electrically powered mine the mean AMTD was about 70 nmwith a σg of 2.0. The thoron (220Rn) WL was similar to the 222Rn WL in the electric poweredmine but less than the 222Rn WL in the diesel powered mine.
(675) Butterweck et al. (1992) carried out activity size measurements in undergroundmines in Germany with a low pressure cascade impactor and a high volume impactor.
Measurements were made at a uranium mine (Groβ-Schloppen), an iron mine (Salzgitter) andat a barite mine (Bad Lauterberge). The activity size distribution of 212Pb could beapproximated by a unimodal log-normal distribution described by the AMAD and σg. During
working hours mean values of the AMAD of 212Pb ranged from 150 – 290 nm with a σgranging from 2 – 3.1. For the Barite mine of Bad Lauterberge, the mean value AMAD of212
Pb was 290 nm during working hours but increased to 400 nm outside working hours.
Measurements were also carried out at a disused silver mine at Lautenthal, which was open to
tourists; the mean value of AMAD was 310 nm (range: 270 – 340 nm) and the σg was 2.4(range: 2.1 – 3.6). In most of these mines, the activity size distributions of the accumulation
mode of 212Pb were broadly similar to the corresponding size distribution of the 222Rn
progeny, 214Pb/214Bi.
(676) The activity size distribution for thoron (220Rn) progeny assumed for the mining
environment is given in Table 12-5. These values are the same as those assumed for radon(222Rn) progeny for mine (Table 12-4) apart from assuming a lower unattached fraction.
Because of the longer half-life of 212Pb, more of the lead is likely to be attached. However,the value of fp also depends upon the ventilation rate; higher unattached fractions are
expected for high ventilation rates.
Reference values for regional deposition of inhaled 222Rn and 220Rn progeny aerosols
221

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8840
8841
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8843
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8845
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8847
8848

Radon (222Rn) progeny(677) The aerosol distributions for the attached 222Rn progeny (218Po, 214Pb and 214Bi) in
the ambient air are given in Table 12-4 for indoor workplaces and mines. Taking account of
hygroscopic growth, the assumed aerosol characteristics of the attached progeny in the
respiratory tract are given in Table 12-6. The unattached mode of the short-lived 222Rn
progeny (i.e. of 218Po and 214Pb) is assumed to have an AMTD of 0.9 nm with σg = 1.3, andunit density and shape factor for both exposure scenarios (Section 12.4.1.1). Table 12-7 gives
the corresponding regional depositions in the respiratory tract for each mode of the assumed
aerosol distribution of 222Rn progeny.
Table 12-6. Attached aerosol characteristics in the respiratory tract for 222Rn progeny
Exposure
scenario

Indoorworkplace
Mine
8849
8850
8851
8852
8853
8854

a
b

σgi b

2.0
2.0
2.0

Indices i = ‘Nucl.’ and ‘Acc.’ represent the nucleation and accumulation modes respectively.
σgi = geometric standard deviation of mode i.

Table 12-7. Deposition of inhaled 222Rn progeny aerosols in respiratory tract regions. Values
are given for each mode of the assumed aerosol distribution for indoor workplaces and mines.
Exposure scenario

Modea

All
Indoor workplace

Unatt.
Nucl.
Acc.
Acc.

Mine
8855
8856
8857
8858
8859
8860
8861
8862
8863
8864
8865
8866
8867
8868

Attached aerosol characteristics in the respiratory tract
Modea, i
AMADi Density,
Shape
AMTDi
(nm)
ρi
(g factor, (nm)
χi
cm-3)
Nucl.
48
1.0
1.0
48
Acc.
427
1.0
1.0
427
Acc.
197
0.7
1.0
250

a
b

Deposition in regions (%)(b)
ET1
ET2
BB
53.33
28.71
7.585
4.458
2.401
1.084
8.643
4.654
0.52893.150
1.696
0.4087

bb
8.633
7.627
1.540
2.164

AI
0.3920
31.79
9.04
9.95

Total
98.65
47.36
24.41
17.37

‘Unatt.’ = unattached mode, ‘Nucl.’ = nucleation mode, and ‘Acc.’ = accumulation mode.
The degree of precision of the values is given for computational purposes and does not reflect thecertainty with which they are known.

Thoron (220Rn) progeny(678) The aerosol distributions for the attached thoron progeny (212Pb and 212Bi) in theambient air are given in Table 12-5 for indoor workplaces and mines. Taking account of
hygroscopic growth, the assumed aerosol characteristics of the attached progeny in the
respiratory tract are given in Table 12-8. The unattached mode of the short-lived 220Rn decay
product, 212Pb is assumed to have an AMTD of 0.9 nm with σg = 1.3, and unit density andshape factor for both indoor workplaces and mines. Table 12-9 gives the corresponding
regional depositions in the respiratory tract for each mode of the assumed aerosol distributionof 220Rn progeny.

222

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
8869
8870

Table 12-8. Attached aerosol characteristics in the respiratory tract for 220Rn progeny
Exposure
scenario
Indoorworkplace
Mine

8871
8872
8873
8874
8875
8876

a
b

σgi b
2.0
2.0
2.0

Indices i = ‘Nucl.’ and ‘Acc.’ represent the nucleation and accumulation modes respectively.
σgi = geometric standard deviation of mode i.

Table 12-9. Deposition of inhaled 220Rn progeny aerosols in respiratory tract regions. Values
are given for each mode of the assumed aerosol distribution for indoor workplaces and mines.
Exposure scenario

Modea

All
Indoor workplace

Unatt.
Nucl.
Acc.
Acc.

Mine
8877
8878
8879
8880
8881
8882
8883
8884
8885
8886
8887
8888
8889
8890
8891
8892
8893
8894
8895
8896
8897
8898
8899
8900
8901
8902
8903
8904
8905

Attached aerosol characteristics in the respiratory tract
Modea, i
AMADi Density,
AMTDi
ρi Shape
-3
(nm)
(nm)
(g cm )
factor, χi
Nucl.
64
1.0
1.0
64
Acc.
340
1.0
1.0
340
Acc.
197
0.7
1.0
250

a
b

Deposition in regions (%)b
ET1
ET2
BB
53.33
28.71
7.585
3.701
1.993
0.895
6.335
3.411
0.467
3.150
1.696
0.4087

bb
8.633
6.231
1.768
2.164

AI
0.3920
26.79
9.35
9.95

Total
98.65
39.60
21.33
17.37

‘Unatt.’ = unattached mode, ‘Nucl.’ = nucleation mode, and ‘Acc.’ = accumulation mode.
The degree of precision of the values is given for computational purposes and does not reflect thecertainty with which they are known.

Inhalation of radon gas(679) The biokinetic model for radon gas described in Section 12.4.3.2 is used to calculate
doses from inhalation of radon gas. Although, radon is chemically inert, the radon gas can beabsorbed into the blood stream from the lung, where it moves rapidly within the body.
Radon gas absorbed to pulmonary blood is distributed in arterial blood to tissues and is thentransferred from tissue to venous blood. The gas is carried in the venous blood to pulmonary
blood where some of it exhaled, while the rest returns to artery blood and the cycle continues.
The transfer rates between blood and tissues depend on blood flow rates, tissue and blood
volumes, and on the relative solubility of radon in tissues and blood represented by tissue-toblood partition coefficients. Transfer rate constants from lung air-to-blood, blood-to-tissues,
tissues-to-blood, and blood-to-lung air are given in Section 12.4.3.2. Equilibrium
concentrations in tissues, blood and lung air are reached for continuous chronic exposure to agiven radon concentration. The time it takes for 222Rn to reach equilibrium concentrations intissues varies from several minutes to a few days depending upon their blood supply and thetissue-to-blood partition coefficient. However, the value of the equilibrium concentration of
222
Rn in a tissue can be calculated directly from the ambient concentration, the tissue-to-blood
partition coefficient, and the blood-to-air partition coefficient.
(680) The equivalent doses to regions of the respiratory tract arising from the radon gas
within the airways are calculated assuming that the radon gas within the airways equilibrates
rapidly with the ambient concentration (Section 12.4.3.2). However, Absorbed Fractions(AFs) have not been calculated for a source consisting of the volume of the gas within the
airways. Because there is little loss of energy within the air in the airways, the AFs for nonpenetrating radiations can be approximated by assuming the activity in the volume of the gas
within the airways can be replaced by the same activity uniformly deposited on the surface(‘surface’ in ET1 and ET2, ‘mucus layers’ in BB and bb, ‘AI’ in AI). For this purpose, Table

223

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
8906
8907
8908
8909
8910
8911

12-10 gives reference volumes of the respiratory tract regions for reference worker (ICRP,
1994).
Table 12-10. Reference volumes of respiratory tract regions for calculating doses from gases
within the airways for Reference worker a,b
Region
ET1
ET2
BB
bb
AI

8912
8913
8914
8915
8916
8917
8918
8919
8920
8921
8922
8923
8924
8925
8926
8927
8928
8929
8930
8931
8932
8933
8934
8935
8936
8937
8938
8939
8940
8941
8942
8943
8944
8945
8946
8947
8948

a
b

Volume (m3)2.500E-06
3.375E-05
3.901E-05
6.265E-05
3.720E-03

Values given to four significant figures for precision in calculation.
Taken from ICRP Publication 68; Table A.1, page 23. In ICRP Publication 68 there is a transcript error
for the reference volume of bb; this has been corrected here.

12.4.2. Ingestion(681) Radon is soluble in water, and if high concentrations are found in drinking water thismay be an important source of exposure. Volunteer experiments have shown that radon isreadily absorbed from the alimentary tract into blood (Section 12.4.3.1). Kursheed (2000)
assumed that ingested radon follow the pathway of water out of the stomach and is absorbed
to blood only via the small intestine. However, important issues relating to the dosimetry ofradon gas from ingestion relate to the residence time of radon in the stomach and the extent towhich radon diffuses into the wall of the stomach. As a result of different assumptions
regarding these two issues published estimates of dose to the stomach wall per unit intake ofingested 222Rn vary by a factor of about 200 (von Döbeln and Lindell, 1964; Hursh et al.,
1965; Suomela and Kahlos, 1972; Crawford-Brown, 1989; Brown and Hess, 1992; Harleyand Robbins, 1994; Sharma et al., 1996; NAS, 1999; Khursheed, 2000). The rate of removalof radon from the stomach assumed in the dose calculations has varied from a few minutes toa few hours. The following approaches illustrate the variety of assumptions that have been
made concerning accumulation of radon in the stomach wall. Hursh and coworkers (1965)
assumed that the stomach wall contains radon at the same concentration as occurs in thestomach contents at all times following ingestion and that the radon is uniformly distributedin the wall. A committee of the U.S. National Academy of Sciences (NAS, 1999) assumed
that the time-integrated concentration of radon at the depth of the radiosensitive cells in thestomach wall is 30% of the time-integrated concentration in the contents. Harley and Robbins(1994) assumed on the basis of the structure and secretory properties of the stomach wall thatany radon that diffuses from the contents into the wall does not reach a depth at which thealpha emissions could irradiate the stem cells. Kursheed (2000) pointed out that improved
fits were obtained between the model predictions and the data of Hursh et al. (1965) if the siteof absorption into blood is only the small intestine.
(682) The biokinetic model for radon gas following ingestion assumed in this report isdescribed in Section 12.4.3.2. In this model it is assumed that radon gas does not diffuse
from Stomach contents to Stomach wall but that radon is absorbed to blood via the small
intestine.
12.4.3. Biokinetic model for radon gas

224

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
8949
8950
8951
8952
8953
8954
8955
8956
8957
8958
8959
8960
8961
8962
8963
8964
8965
8966
8967

12.4.3.1. Summary of the database(683) The noble gases are chemically inert but are absorbed to blood from the lungs or
gastrointestinal tract and retained in systemic tissues to some extent, due in part to theirsolubility in blood and tissues. Much of the gas that reaches blood is cleared by the lungs in asingle pass, but a portion is partitioned between the blood and tissues. The rate of transfer ofthe gas from blood to a tissue can be estimated on the basis of the fraction of cardiac output
received by the tissue. The rate of return from a tissue to blood depends on both the blood
perfusion rate and the relative solubility of the gas in blood and the tissue, represented by agas-specific tissue-to-blood partition coefficient.
The partition coefficient for two
compartments is defined as the ratio of the concentrations of the gas in the compartments at
equilibrium. Some experimentally determined tissue-to-blood partition coefficients for thenoble gases radon, xenon, and krypton are listed in Table 12-11. Half-times for the buildup
or washout of these gases are a few minutes for tissues with a rich blood supply and low tomoderate partition coefficients but are much greater for fatty tissues because of their poor
blood supply and high tissue-to-blood partition coefficient. Within an hour after acute intake
or the start of continuous intake of radon, xenon, or krypton, body fat contains most of thesystemic content.
Table 12-11. Partition coefficients for radon, xenon, and kryptona
Organ/blood
Fat
MuscleBone
Kidney
Liver
Brain
Heart
TestesGI tract
Lung
Spleen
Skin

Radon
11
0.36
0.36b
0.66
0.71
0.72
0.51
0.43
0.70b
0.70b
0.70b
0.36b

Xenon
8-10
0.70
0.41
0.65
0.70
0.75

Blood/air

0.43

0.18

Krypton
5.50
1.09
∼1.0
1.1
~1.0
0.85

0.80
0.70

0.06

a

Nussbaum and Hursh, 1957; Conn, 1961; Kirk et al., 1975; Bell and Leach,
1982; Peterman and Perkins, 1988; NAS, 1999; Khursheed, 2000.
b
Values assigned by Bernard and Snyder (1975).
8968
8969
8970
8971
8972
8973
8974
8975
8976
8977

(684) The partition coefficients for radon given in Table 12-11 were derived from radonsolubility coefficients quoted by Bernard and Snyder (1975), which in most cases were basedon in vivo rat data of Nussbaum and Hursh (1957). The values for bone and skin were basedon radon solubility in physiological saline.
Ingestion of 222Rn by volunteers(685) A number of investigators have used measurements of 222Rn in breath or externalmeasurements of the short-lived chain member 214Bi to estimate whole-body retention ofradon in human subjects after ingestion of elevated levels in water or other material

225

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
8978
8979
8980
8981
8982
8983
8984
8985
8986
8987
8988
8989
8990
8991
8992
8993
8994
8995
8996
8997
8998
8999
9000
9001
9002
9003
9004
9005
9006
9007
9008
9009
9010
9011
9012
9013
9014
9015
9016
9017
9018
9019
9020
9021
9022
9023
9024
9025

(Vaternahm, 1922; Fernau and Smereker, 1933; Meyer, 1937; Anderson and Nilsson, 1964;
von Dobeln and Lindell, 1964; Hursh et al., 1965; Suomela and Kahlos, 1972; Gosink et al.,
1990; Brown and Hess, 1992). Reported rates of loss of radon from the body are variable,
probably due in large part to differences in experimental conditions such as the timing of
intake of radon relative to meals, the level of physical activity of the subjects after intake ofradon, and the length of the observation period. Retention half-times in the range 30-70 min
have been reported in several studies involving relatively short observation periods. Multiple
retention components with half-times varying from a few minutes to several hours have been
determined in some studies with relatively long observation periods.
(686) Hursh et al. (1965) used periodic measurements of breath to estimate total-bodyretention of 222Rn following acute intake of 222Rn in water by each of two subjects on two
occasions. In three of the four individual experiments the radon was ingested two hours after
a normal light breakfast. In the fourth experiment the radon was ingested 10 min after a heavy
breakfast. Retention was longer in the fourth experiment than in the first three, presumably
due to a longer retention time in the full stomach. Retention of radon in the subjects withempty stomach could be expressed as a sum of three exponential terms corresponding to halftimes of about 11 min (61%), 19 min (34%), and 3 h (5%). Retention in the subject with fullstomach could be expressed as a sum of three exponential terms corresponding to half-timesof about 12 min (39%), 58 min (51%), and 5 h (10%). Hursh and coworkers interpreted thedata as indicating that much of the ingested radon mixes with the stomach contents, diffusesout through the stomach walls into the splanchnic venous blood system, and passes throughthe liver and up into the right heart to the lung where much of the absorbed amount is rapidly
lost in the expired air. Uptake of radon by systemic tissues was assumed to be divided mainly
among three pools: liver, fat, and other. Fat was estimated to contain only a small portion of
the systemic burden in the early minutes after intake but a major portion after 2-3 h.
(687) Suomela and Kahlos (1972) used external measurements of the 222Rn chain member
214
Bi to estimate whole-body retention of radon in 10 healthy adult male subjects who
ingested radon-rich water as a single intake. A single exponential function with biologicalhalf-time in the range 30-50 min was found to describe the elimination of 222Rn reasonably
well in some cases over observation periods of up to about 6 h. In other cases a second
component with half-time 1.5-2 h was evident within the 6-h observation period. Suomela
and Kahlos compared their findings with results from earlier studies of retention of 222Rn
ingested in water by human subjects (Andersson and Nilsson, 1964; Döbeln and Lindell,
1964; unpublished study by Mays, 1972; Hursh et al., 1965). The retention curves determinedby Hursh et al. (1965) for a full and empty stomach bounded the retention curves determinedin other studies over the first 6 h after intake.
(688) Gosink et al. (1990) used breath measurements to estimate the rate of loss of 222Rn
from a 51-year-old male subject (1.96 m, 112 kg) in different experiments involving
consumption of water with a moderately high natural concentration of 222Rn. During a periodof relatively high physical activity the subject eliminated virtually all the ingested 222Rn
during the first 4 h after intake. During mild activity the biological half-time was 45-65 min.
For a sedentary or sleeping period a biological half-time was estimated as 11.2 h for a
substantial portion of the ingested radon. For the sedentary case the subject exhaled <3% ofingested 222Rn per hour after the first hour.
(689) Brown and Hess (1992) conducted 41 tests on 38 human subjects, ages 9-85 y, tomeasure elimination rates of 222Rn in expired breath following acute intake of 222Rn in
drinking water. The levels of physical activity of the subjects ranged from inactive tomarathon level. The percentage of elimination of 222Rn from the body during the first 30 min
226

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9026
9027
9028
9029
9030
9031
9032
9033
9034
9035
9036
9037
9038
9039
9040
9041
9042
9043
9044
9045
9046
9047
9048
9049
9050
9051
9052
9053
9054
9055
9056
9057
9058
9059
9060
9061

after intake ranged from 12 to 68%. The elimination rate showed a moderate correlation withthe time passed since eating. Estimated retention half-times ranged from 17 to 400 min.
Inhalation of inert gases by volunteers(690) In a series of experiments, Harley and coworkers (1951, 1994) studied the retentionof inhaled radon by subjects following exposures to constant, elevated concentrations ofradon in air for periods up to 8.5 h. Measurements of 222Rn in periodic breath samples after
the end of exposure were used to infer the rate of loss of 222Rn from the body. About thesame peak total-body content of radon (~850 Bq) was estimated following exposure for 8.5 h
at an air concentration of 25.9 Bq/L and for 7 h at 22.2 Bq/L, suggesting that saturation may
have been approached. Following both the 7-h and 8.5-h exposures the activity remaining in
the body at the end of exposure showed five distinct components of retention. In the moredetailed study involving exposure for 8.5 h, about 8% of the total expired radon was removed
with a half-time of 23 s, 9% with a half-time of 4.5 min, 18% with a half-time of 41 min,
32% with a half-time of 3.4 h, and 33% with a half-time of 18 h. These retention half-times
are broadly similar to half-times observed in human subjects following inhalation of xenon or
krypton (Susskind et al., 1977; Ellis et al., 1977).
(691) Susskind et al. (1977) used in vivo measurements to estimate retention of inhaled
127
Xe in 12 human subjects. Five components of retention with average biological half-timesof 21.7 s, 3.05 min, 0.40 h, 2.71 h, and 10.4 h were determined. The half-time of the slowest
component of clearance ranged from 7.4 h to 17.0 h and correlated highly with total-body fat
as a percent of body weight (Figure 12-5). The mean half-time (+/- standard deviation) of thiscomponent for five subjects with body fat representing less than one-third of total-bodyweight was 8.4 +/- 0.7 h. On average the slowest component of clearance represented
approximately 13% of the retained activity, excluding the rapid clearance represented by theretention components with half-times 21.7 s and 3.05 min.
(692) Ellis et al. (1977) studied total-body retention of 79Kr in 16 subjects by whole-bodyexternal counting following a 10-min or 30-min inhalation period. The retention data wereresolved into a five-component exponential curve with average half-times of 21.5 s, 4.74 min,
0.33 h, 2.41 h, and 7.0 h. The last three retention components represented on average 61.7%,
29.6%, and 9.4% of the retained activity, excluding the rapid clearance represented by theretention components with half-times of 21.5 s and 4.74 min. The half-time of the long-term
component ranged from about 4.2 h to 9.6 h and correlated significantly with the estimatedpercentage of total body fat (Figure 12-5). The mean half-time (+/- standard deviation) forsix subjects with body fat representing less than one-third of body weight was 5.5 +/- 0.7 h.

227

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION

9062
9063
9064
9065
9066
9067
9068
9069
9070
9071
9072
9073
9074
9075
9076
9077
9078
9079
9080
9081
9082
9083
9084
9085
9086
9087
9088
9089
9090
9091
9092
9093
9094
9095

Figure 12-5. Relation of body fat (% of body weight) and long-term clearance half-time of
inhaled Xe or Kr. Data on Xe from Susskind et al. (1977). Data on Kr from Ellis et al. (1977).

Loss of noble gas from the body other than through exhalation(693) Loss of radon or other noble gases through skin, urine, or faeces is expected to besmall compared with loss through exhalation. Limited measurements of radon or its progeny
in urine following ingestion of high levels of radon in drinking water indicated that urinary
excretion did not represent a significant mode of loss (Hursh et al., 1965; Gosink et al., 1990).
On the basis of a mechanistic biokinetic model of inert gases in the human body, Peterman
and Perkins (1988) estimated that loss of xenon through the skin amounts to about 0.6% of its
loss through the lungs.
12.4.3.2. Biokinetic model for systemic radon(694) Compartmental biokinetic models have been developed for a number of inert gases,
including radon, on the basis of physical laws governing transfer of a non-reactive and solublegas between materials (Kety, 1951; Bell and Leach, 1982; Peterman and Perkins, 1988;
Sharma et al., 1997; NAS 1999; Khursheed 2000; Yu and Kim, 2004). The biokinetics ofsuch a gas is assumed to be determined by the blood-to-air partition coefficient and the blood
perfusion rates, tissue-to-blood partition coefficients, and volumes of the tissues represented
by the compartments of the model. As depicted in the standard modelling approach, an inert
gas entering the lung air after inhalation or entering pulmonary blood after absorption fromthe gastrointestinal contents equilibrates instantly between lung air and pulmonary blood,with relative concentrations in the two pools determined by their volumes and blood-to-air
partition coefficients. Gas retained in the pulmonary blood is distributed in arterial blood totissues in proportion to the percentage of cardiac output received by each tissue. The transfer
rate from a tissue to venous blood is determined by the blood perfusion rate, the volume of
the compartment, and the tissue-to-blood partition coefficient. The gas is carried in thevenous blood to the pulmonary blood. The cycle continues until the body burden is depleted
due to exchange between pulmonary blood and lung air and loss from the body in expired air.
(695) For a given tissue, a set of differential equations can be derived by considerations ofmass balance and equilibrium. As an example, consider a systemic tissue that receives blood
only from the arterial pool and leaves in the venous stream. The rate of change of the activity

228

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9096
9097
9098
9099
9100
9101
9102
9103
9104
9105
9106
9107
9108
9109
9110
9111
9112
9113
9114
9115
9116
9117
9118
9119
9120
9121
9122
9123
9124
9125
9126
9127
9128
9129
9130
9131
9132
9133
9134
9135
9136
9137
9138
9139

of inert gas in a tissue is Fi (CB-A – CB-V), where Fi is the blood flow rate (L min-1) through thesystemic tissue, CB-A is the activity gas concentration (Bq L-1) in non-pulmonary arterial
blood and CB-V is the activity gas concentration in non-pulmonary venous blood. In thestandard modeling approach it is assumed that the perfusion of the gas in tissues isinstantaneous, allowing equilibrium to achieve between venous blood and tissue such that CBV = Ci/Pi, where Ci is the activity concentration of the gas in the tissue and Pi is the tissueblood partition coefficient. Thus, for a given organ the differential equation describing therate of change of the activity of gas Qi in a tissue, is:


dQi
C 
= Fi  C B − A − i  − λ r Qi
dt
Pi 


(Eq. 12-5)

where λr is the radioactive rate constant for the inert gas. To express the above equation interms of activity of gas, Q, it can be rewritten as:dQi
FF= i QB − A − i Qi − λ r Qi
dt
VB − A
Pi Vi(Eq. 12-6)

where VB-A is the volume of the non-pulmonary arterial blood and Vi is the volume of thetissue. So the transfer rate constant from arterial blood to tissue is Fi/VB-A and the transfer
rate constant from tissue to venous blood is Fi/(PiVi). The blood flow rate (Fi) through asystemic tissue, i is given by the product of the cardiac output and the fraction of the cardiac
output going to tissue, i (ICRP, 2002). The volume of a systemic tissue is calculated from its
mass and specific gravity.
(696) The biokinetic model for radon used in this report is based largely on the theoreticalconsiderations summarised above but includes some empirical features and simplifications.
As a first step, a detailed biokinetic model involving three blood compartments representing
pulmonary, arterial, and venous blood and 20 compartments representing systemic tissues
was developed for radon on the basis of these theoretical considerations. That model was thensimplified for use in this report by dividing blood into two rather than three compartments,
pooling several tissue compartments with broadly similar time-dependent radon
concentrations, and replacing the theoretical model of instantaneous exchange of radon
between lung air and pulmonary blood with a first-order system consistent with the ICRP’s
general modelling approach for inhaled activity. Also, the theoretical considerations asapplied to bone were replaced by a dosimetrically cautious bone model involving exchange ofradon between blood and bone surfaces.
(697) The structure of the model used in this report is shown in Figure 12-6. Baselinetransfer coefficients are listed in Table 12-12.
(698) Blood is divided into arterial and venous blood (Blood-A and Blood-V,
respectively). These compartments are assumed to represent 27%, and 73%, respectively, ofthe total blood volume based on reference sizes of blood pools summarized in ICRP
Publication 89 (2002). The reference total blood volume is 5.3 L in the adult male and 3.9 L
in the adult female (ICRP, 2002).
(699) Fat is represented as two compartments with equal volumes but different blood
perfusion rates as a way of depicting the two phases of relatively long-term retention (several
hours) observed in human subjects following inhalation of radon or radioisotopes of xenon or

229

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9140
9141
9142
9143
9144
9145
9146
9147
9148
9149
9150
9151
9152
9153
9154
9155
9156
9157
9158
9159
9160
9161
9162
9163
9164
9165
9166
9167
9168
9169
9170
9171
9172
9173
9174
9175
9176
9177
9178
9179
9180
9181
9182
9183
9184

krypton. The blood perfusion rate of Fat 1 is assumed to be four times higher than that of Fat
2, which implies that the removal half-time from Fat 2 is four times greater than the removal
half-time from Fat 1.
(700) For continuous inhalation of radon, it is assumed that the activity concentration in
respiratory tract (RT) air rapidly reaches equilibrium with the activity concentration in theenvironment, Cenv. The transfer rate from RT air to environment, λ is assumed to be 2600 d-1(half-time 23 s). The removal half-time of 23 s is based on observed half-times for the rapid
phase of exhalation of radon, xenon, or krypton by human subjects immediately after a periodof continuous inhalation (Harley et al., 1951; Susskind et al., 1977; Ellis et al., 1977). The
removal half-time does depend on breathing rate but for dosimetry purposes it is assumed tobe constant. The rate at which activity enters the RT air space is assumed to be λ Cenv VRT-air(Bq d-1), where VRT-air is the average volume of the RT air space (3.858 L for male, ICRP,
1994). In order to use the model to calculate the number of disintegrations in the respiratory
tract (RT) air space, this rate is partitioned to each region of the HRTM according to its
fractional volume (Table 12-10).
(701) It is assumed that the radon in RT air diffuses to Blood-A rapidly, allowing
equilibrium to achieve between Blood-A and RT air such that CB-A = CRT-air Pb-air, where Pb-air
is the blood to air partition coefficient, (Table 12-11) and CRT-air is the activity concentrationin RT air. On the basis of mass balance and equilibrium the rate of change of activity in the
RT air is given by:
dQ RT − air= λC envV RT − air − λQ RT − air + F (C B −V − C RT − air Pb − air ) − λ r Q RT − airdt(Eq. 12-7)

where F (L min-1) is the cardiac output. To express the above equation in terms of activity ofgas, Q, it can be rewritten as:
dQ RT − air
F Pb − air
F
Q RT − air − λ r Q RT − air
Q B −V −= λC envV RT − air − λQ RT − air +dt
V B −VV RT − air(Eq. 12-8)(702) From equation (4.8) it can be seen that the transfer rate constant from Blood-V to
RT-air is F/VB-V and the transfer rate constant from RT-air to Blood-A is F Pb-air/VRT-air.
(703) Radon ingested in drinking water or other material is transferred from Stomach
contents to Small intestine contents at a material-specific stomach emptying rate. The default
transfer coefficient from Stomach contents to Small intestine contents are reference values for
total diet (ICRP, 2002, 2006): 20.57 d-1 for adult males and 15.16 d-1 for adult females.
(704) Radon is transferred from Small intestine contents to Liver at the rate 5994 d-1. This
corresponds to an absorption fraction of 0.999 based on a reference transfer coefficient of 6 d1
from the small intestine contents to the right colon contents (ICRP, 2002, 2006).
(705) With exceptions described later, derivations of transfer coefficients between
systemic compartments are based on the blood flow rates, compartment volumes, and tissueto-blood partition coefficients listed in Table 12-13. The blood flow rates are taken from
ICRP Publication 89 (2002). The compartment volumes are based on reference tissue masses
for adults (ICRP, 2002), together with the following specific gravities based on information
summarized in ICRP Publication 23 (1975) and Publication 89 (2002): fat, 0.92; red marrow,
1.0; all other soft tissues, 1.04. The tissue-to-blood partition coefficients are based on
estimates listed in Table 12-11. A rounded partition coefficient of 0.4 for Other was based on

230

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9185
9186
9187
9188
9189
9190
9191
9192

9193
9194
9195
9196
9197
9198
9199
9200
9201
9202
9203
9204
9205
9206
9207

the estimate of 0.36 for skeletal muscle, which represents much of the volume of Other. The
specific gravity and tissue-to-blood partition coefficient for red marrow are based onreference masses of active marrow and total marrow given in ICRP Publication 89 (2002) andthe assumptions that red marrow is composed of active marrow plus fat and represents half
the mass of total marrow. In other words, the specific gravity and tissue-to-blood partition
coefficient for red marrow were calculated assuming red bone marrow is composed of about
40% fat (ICRP, 1975).

Figure 12-6. Structure of the biokinetic model for systemic radon(706) The derivation of transfer coefficients is illustrated for the reference adult male.
Radon is cleared from Blood-A at the rate 6.5 L min-1 x 1440 min d-1 / 1.431 L = 6541 d-1,
where 1.431 L = 0.27 x 5.3 L is the volume of Blood-A. Radon is transferred from Blood-V
to lung air at the rate 6.5 L min-1 x 1440 min d-1 / 3.869 L = 2419 d-1, where 3.869 L = 0.73 x
5.3 L is the volume of Blood-V. The transfer coefficient from Blood-A to Kidneys, forexample, is 0.19 x 6541 d-1 = 1243 d-1, where 0.19 is the fraction of cardiac output received
by the kidneys in the reference adult male. The transfer coefficient from Kidneys to Blood-V
is 1440 min d-1 x 0.19 x 6.5 L min-1 / (0.298 L x 0.7) = 8525 d-1, where 0.298 L is the volumeof the kidneys and 0.7 is the kidneys-to-blood partition coefficient.
(707) Tissue compartments other than Liver receive radon only from Blood-A. In addition
to Blood-A, Liver receives a portion of outflow from Other, representing radon that leaves thesplanchnic tissues, as well as radon absorbed from the alimentary tract following its

231

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9208
9209
9210
9211
9212
9213
9214
9215
9216
9217
9218
9219
9220
9221
9222
9223
9224
9225
9226
9227
9228
9229
9230
9231
9232
9233
9234
9235
9236
9237
9238
9239
9240
9241
9242
9243
9244
9245
9246
9247
9248
9249
9250
9251
9252
9253
9254
9255

ingestion. Activity leaving tissue compartments is assigned to Blood-V, except that the
portion of outflow from Other representing outflow from splanchnic tissues is assigned toLiver. The fraction of outflow from Other assigned to Liver is 19/(19+46) = 19/65, based on
estimated blood flows of 19% and 46%, respectively, of cardiac output through splanchnic
and non-splanchnic tissues within Other.
(708) As a dosimetrically cautious approach, radon depositing in bone is assigned to bone
surface. Transfer coefficients from Blood-A to Trabecular bone surface and Cortical bone
surface are based on the reference blood flow rates of 0.9% and 0.6% to trabecular andcortical bone, respectively expressed as a % of cardiac output (ICRP, 2002). Transfer
coefficients from these bone surface compartments to Blood-V were not derived by the same
methods as applied to other tissue compartments due to difficulties in determining meaningful
volumes and partition coefficients for bone surface. Rather, the transfer coefficient from eachbone surface compartment to Blood-V is taken as 100 d-1, which is the value estimated in
ICRP Publication 67 for radon produced on bone surface by radioactive decay of radiumisotopes.
(709) Figure 12-7 compares model predictions derived from the baseline parameter values
in Table 12-12 with observations of total-body retention in adult male subjects exposed
acutely to elevated levels of 222Rn in drinking water. Two sets of predictions are shown, one
based on relatively fast transfer of radon from the stomach to the small intestine (T1/2 = 15min), and one based on relatively slow transfer (T1/2 = 1 h). The predicted total-body retention
pattern based on a half-time of 15 min in the stomach is reasonably similar to the retention
pattern observed for subjects who ingested radon two hours after a light breakfast (Hursh etal., 1965). The predicted retention pattern based on a half-time of 1 h in the stomach isreasonably similar to the pattern observed by the same investigators for a subject who
ingested radon 10 min after a heavy breakfast.
(710) Figure 12-8 compares model predictions with observations of the rate of exhalationof 222Rn by an adult male following exposure to a constant, elevated concentration (25.9
Bq/L) of radon in a closed room for 8.5 h (Harley et al., 1951). The rate of exhalation ofradon at the end of the 8.5-h exposure was 132 Bq/min. This indicates a radon inhalation rateof 132 Bq/min and is consistent with the breathing rate (Br) of 5 L air/min estimated byHarley and coworkers. A transfer rate λ of 2600 d-1 (1.8 min-1) from RT air to environment isestimated from the fastest component (half-time of 23 s) of the exhalation rate of radon
determined in the human study. The estimated volume of lung air involved in the radon
exchange with blood is VL-air=Br/λ=2.8 L. Based on a lung air volume of 2.8 L, the transfer
coefficient from RT air to Blood-A is F Pb-air/ VL-air = 1437 d-1, where F is cardiac output inblood volumes per day and Pb-air is the blood-to-air partition coefficient. This case-specificestimate of the transfer coefficient from RT-air to Blood-A was used in the model simulation
rather than the baseline value 1043 d-1 listed in Table 12-12. All other model parameters wereassigned their baseline values. A radon inhalation rate of 190,000 Bq/d (132 Bq/min) was
assumed.
12.4.3.3. Treatment of radioactive progeny(711) The radon isotopes addressed in this report as parent radionuclides are 222Rn, 220Rn,
and 219Rn. Their radioactive progeny considered in the determination of dose coefficients areisotopes of lead, polonium, bismuth, and thallium. Radioisotopes of mercury, astatine, andradon also appear in the 222Rn chain, but their contributions to tissue doses following intakeof 222Rn are negligible.
232

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9256
9257
9258
9259
9260
9261
9262
9263
9264
9265
9266
9267
9268

(712) The systemic models for lead, polonium, bismuth, and thallium as radon progeny arebased on their characteristic systemic models as modified for their application as lead progeny(see the section on lead). The following additions are made to their models as lead progeny:
lead, polonium, bismuth, or thallium produced in respiratory tract air (RT-air) is assumed to
be exhaled at the rate 1000 d-1; polonium produced in a blood compartment for which its
biokinetics is not defined is assumed to transfer to the central blood compartment of thepolonium model at the rate 1000 d-1; lead produced in a soft-tissue compartment for which its
biokinetics is not defined is assumed to transfer to the central blood compartment of the leadmodel at the rate 7.39 d-1 (the highest transfer rate from tissues to blood in the lead model);and bismuth produced in a soft-tissue compartment for which its biokinetics is not defined isassumed to transfer to the central blood compartment of the bismuth model at the rate 66.542
d-1 (the highest transfer rate from tissues to blood in the bismuth model).
Table 12-12. Transfer coefficients in the systemic model for radon

From
Environment
RT airBlood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Blood-A
Fat 1
Fat 2
Kidneys
Liver
Trab bone surface
Cort bone surface
Red marrow
Other
Other
Blood-V
RT airStomach Content
SI Content

9269
9270
9271
9272
9273
9274

To
RT airEnvironment
Fat 1
Fat 2
Kidneys
Liver
Trab bone surface
Cort bone surface
Red marrow
Other
Blood-V
Blood-V
Blood-V
Blood-V
Blood-V
Blood-V
Blood-V
Blood-VLiver
RT airBlood-ASI Content
LiverTransfer coefficient (d-1)
Adult male
Adult female
(a)
(a)
2600
2600
261.6
548.6
65.41
137.2
1243
1372
425.2
524.4
58.9
72.6
39.3
48.4
196.2
242.0
4252
5123
4.48
5.68
1.12
1.42
8525
7803
1970
586.1
100
100
100
100
34.1
42.0
260.3
302.7
107.5
149.8
2419
2984
1043
1043
20.57
15.16
5994
5994

(a) The rate at which activity enters the respiratory tract (RT) air space is assumed to be λ Cenv VRT-1-1
air (Bq d ), where λ is the transfer coefficient from environment to RT air space (2600 d ),-1
Cenv is the concentration of radon in the environment (Bq L ), and VRT-air (L) is the averagevolume of the respiratory tract air space (3.858 L for male, ICRP, 1994). This rate ispartitioned to each region of the HRTM according to its fractional volume (Table 12-10).

233

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9275

Table 12-13. Reference blood flow rates, compartment volumes, and blood:tissue
partition coefficients used to derive transfer coefficients.

Compartment
Fat 1
Fat 2
Kidneys
Liver
Arterial
Total
Trabecular bone surface
Cortical bone surface
Red marrow
Other
Blood
Blood-A
Blood-V
Cardiac output (L min-1)

Blood flow ratea(%
ofcardiacoutput)Male
Female
4
6.8
1
1.7
19
17
6.5
25.5
0.9d
0.6d
3
65
---6.5

6.5
27
0.9d
0.6d
3
63.5
---5.9Volumeb
(L)
Male
7.61
7.61
0.298
1.73

Female
9.24
9.24
0.264
1.35

Blood:Tissue
partitioncoefficientc
11
11
0.7
0.7

--1.83
41.35
5.3
1.431
3.869
--

--1.35
29.80
3.9
1.053
2.847
--

--4.5
0.4
-----

a

From ICRP Publication 89 (2002).
Based on reference tissue masses given in ICRP Publication 89 (2002) and specific gravities listed in
the text.
c
See Table 12-11 and discussions in text of partition coefficients for Red marrow and Other.
d
See discussion in text.
b

9276
9277
9278

Figure 12-7. Comparison of model predictions and observations of total-body retention ofradon following its ingestion in drinking water

234

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION

9279
9280
9281
9282
9283
9284
9285
9286
9287
9288
9289
9290
9291
9292
9293
9294
9295
9296
9297
9298
9299
9300
9301
9302
9303
9304
9305
9306

Figure 12-8. Comparison of model predictions and observations of the exhalation rate of radon
following continuous exposure to a high concentration of radon in air for 8.5 hours

12.5.

Dosimetry

12.5.1. Calculation of dose conversion factor arising from the inhalation of radon
progeny.
(713) The effective doses arising from the inhalation of the short-lived radon progeny arecalculated in terms of Sv per PAE exposure, (i.e. in units of Sv per J h m-3 or in units of Sv
per WLM). The intakes of activity of the radon progeny, Ii (in Bq) for a subject exposed to 1
WLM are given by Eq. 12-9. :I i = Ci B t(Eq. 12-9)

where Ci (in Bq m-3) is the activity concentration of the decay product i corresponding to aradon progeny mixture of 1 WL, B (in m3 h-1) is the average breathing rate and t (in h) is the
exposure period of 170 h.
(714) In practice, the activity concentrations of radon progeny will vary with particularenvironmental conditions of exposure. However, Marsh and Birchall (2000) showed that for
intakes of short-lived 222Rn progeny, the equivalent dose to the lung per WLM is relative
insensitive to F (i.e. to the activity ratios of the radon progeny). This is because the WL isdefined in terms of the PAEC and because the fraction of alpha energy absorbed by the target
tissues in the lung is similar for 218Po and 214Po per disintegration. Based on measurementsof the activity concentration of 218Po, 214Pb, and 214Bi carried out indoors (Reineking andPorstendörfer, 1990; Kojima and Abe, 1988) the following activity ratios of 222Rn progeny
are assumed for dosimetry:

235

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9307
9308
9309
9310
9311
9312
9313
9314
9315
9316
9317
9318
9319
9320
9321
9322

Unattached: 218Po : 214Pb : 214Bi = 1 : 0.1 : 0
Attached: 218Po : 214Pb : 214Bi = 1 : 0.75 : 0.6(715) For thoron (220Rn) progeny, the activity ratios assumed are the ones proposed by thecommittee of the National Research Council (NRC, 1991); activity ratios of 212Pb : 212Bi of
1.0:0 and 1.0:0.25 were assumed for the unattached and attached modes respectively. Because
216
Po contributes less than 0.001% to the PAEC, it can be ignored for dosimetry purposes.
(716) The activity concentrations of radon progeny that correspond to a radon progeny
mixture of 1 WL for either the unattached or the attached progeny can be calculated byassuming the above activity ratios and by applying Eq. 12-1. These values are given in Table
12-14.
Table 12-14. Activity concentrations, Ci of a mixture of short-lived radon (222Rn) or thoron(220Rn) progeny that gives 1 WL for either the unattached or the attached progeny
Activity concentration, Bq m-3
Unattached
Attacheda

NuclideRadon (222Rn) progenyb:
218
Po
214
Pb
214
Bi
Thoron (220Rn) progenyc:
212
Pb
212
Bi
9323
9324
9325
9326
9327
9328
9329
9330
9331
9332
9333
9334
9335
9336
9337
9338
9339
9340
9341

2.41 104
2.41 10305.21 103
3.91 103
3.13 103

3.01 10202.94 102
7.36 101a

For simplicity, it is assumed that the activity ratios of the radon progeny for each of the attachedmodes are the same.
b
Activity ratios of 218Po : 214Pb : 214Bi of 1.0:0.1:0 and 1.0:0.75:0.60 are assumed for the unattached
and attached modes respectively.
c
Activity ratios of 212Pb : 212Bi of 1.0:0 and 1.0:0.25 are assumed for the unattached and attachedmodes respectively.

(717) For the average breathing rate, B, the ICRP default value for a reference worker of
1.2 m3 h-1 is assumed for all exposure scenarios (ICRP, 1994). Regarding exposures in amine, this value is similar to the average breathing rate of 1.3 m-3 h-1 estimated from a studyof 620 underground miners carrying out heavy work in a gold mine in South Africa (ICRP
Publication 66, para. B76, ICRP, 1994). It is also consistent with the breathing rates derived
by Ruzer et al. (1995) for personnel (0.9 ± 0.4 m-3 h-1), assistant drillers (1.1 ± 0.5 m-3 h-1)
and drillers (1.4 ± 0.5 m-3 h-1) working underground in a metal mine in Tadjikistan.
(718) The effective dose per WLM arising from the inhalation of the short-lived radon
progeny is calculated by combining the intakes, Ii (derived from Eq. 12-9) with the effective
dose coefficients (Sv per Bq) for the individual radon progeny. The following equation isapplied:39342

E ( Sv per WLM ) = ∑ ∑ I j ,i f pj E j ,i
i =1

9343
9344
9345

(Eq. 12-10)

jwhere index j corresponds to the aerosol mode of the activity size distribution; j=1, 2, and 3
for the unattached, nucleation and accumulation modes respectively. The fpj value is the236DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9346
9347
9348
9349
9350
9351
9352
9353
9354
9355
9356
9357
9358
9359
9360
9361
9362
9363
9364
9365

fraction of the PAEC associated with mode j. The index i corresponds to the inhaled decay
product; in the case of 222Rn progeny, i =1, 2, and 3, which corresponds to 218Po, 214Pb and214
Bi respectively. The symbol Ej,i is the effective dose coefficient (in Sv per Bq) for decay
product i with an activity size distribution for mode j. In the case of 222Rn progeny, theintakes Ij,1, Ij,2 and Ij,3 are the intakes of 218Po, 214Pb and 214Bi respectively, which result in an
exposure of 1 WLM for either the unattached progeny (j=1) or for the attached progeny(j=2,3).
(719) Table 12-15 gives calculated values of the effective dose per unit exposure forindoor workplaces and mines in terms of PAE exposure (mSv per WLM or mSv per mJ h m3
) and in terms of radon gas exposure (Sv per Bq h m-3). For exposures to 222Rn progeny, theunits Sv per WLM can be converted to Sv per Bq h m-3 of 222Rn gas exposure by multiplyingby (F/6.37 105 WLM per Bq h m-3). For exposures to thoron (220Rn) the units Sv per WLM
can be converted to Sv per Bq h m-3 of EEC of 220Rn by multiply by (1/4.68 104 WLM per Bq
h m-3 of ECC of 220Rn).
(720) The committed equivalent doses to organs arising from the inhalation of 222Rn
progeny and from 220Rn progeny are given in the accompanying electronic disk.
Table12-15. Calculated values of effective doses per unit exposure to radon progeny for indoor
workplaces and mines. Dose from inhaling 222Rn or 220Rn gas is excluded.
Place

Unattachedfractiona, fp

Radon (222Rn) progeny:
Indoor workplace
0.1
Mine
0.01
220
Thoron ( Rn) progeny:
Indoor workplace
0.02
Mine
0.005
9366
9367
9368
9369
9370
9371
9372
9373
9374
9375
9376
9377
9378
9379
9380
9381
9382
9383
9384
9385

Fb

0.4
0.2

Effective dose per unit exposurec
mSv per mSv per mJ Sv per
WLM
h m-3
h m-3
21
11

5.9
3.0

Bq

1.3 10-8
d

-

d

a

fp = unattached fraction in terms of the potential alpha energy concentration (PAEC).
F = equilibrium factor.
c
1 WLM = (6.37 105/F) Bq h m-3; 1 WLM = 3.54 mJ h m-3d
In terms of Sv per Bq h m-3 of EEC of 220Rnb

Inhalation of short-lived decay products of actinon 219Rn(721) Because actinon (219Rn) has a very short half-life (4s) it is less able than radon(222Rn; half-life 3.8 d) or thoron (220Rn; half-life 56 s) to escape from the point of where it isformed. As a consequence, exposures to 219Rn and its progeny in the workplace are low andcan generally be ignored. However, there may be some unusual situations where it isappropriate to calculate doses from inhaling 219Rn and its progeny. For example, Crawford(1980) reported that radiological surveys at former uranium ore processing facilities showedthat there were a number of sites with high levels of airborne 219Rn decay products. Further
investigation showed that these sites had been used for the storage of a precipitate, which wasformed during processing pitchblende ore and found to have a relatively high content of 227Ac
and a low content of 226Ra. In such cases, for radiation protection purposes, it is normallysufficient to control exposures on the basis of the intake of 211Pb. This is because the PAE
per unit activity of 211Pb is about 15 times higher or more than for other actinon progeny.
However, for completeness, in the accompanying electronic disk dose coefficients (Sv Bq-1)
are given for both 211Pb and 211Bi. To our knowledge there have been no activity size

237

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9386
9387
9388
9389
9390
9391
9392
9393
9394
9395
9396
9397
9398
9399
9400
9401
9402
9403
9404
9405
9406
9407
9408
9409
9410
9411
9412
9413
9414
9415
9416
9417
9418
9419
9420
9421
9422
9423
9424
9425
9426
9427
9428
9429
9430
9431
9432
9433

measurements of actinon progeny. Dose coefficients have been calculated separately for theunattached, nucleation and accumulation modes with size characteristics (AMTD, σg) equal
to that assumed for 222Rn progeny in indoor work places (Table 12-4 and Table 12-6),
because the half-life of 211Pb (36 minutes) is much closer to that of the 222Rn decay product214
Pb (27 minutes) than that of the 220Rn decay product 212Pb (11 h). For these modes theregional deposition in the respiratory tract are given in Table 12-7.
12.5.2. Inhalation of radon gas(722) The equilibrium effective dose rate for continuous chronic exposure to unit
concentration of 222Rn is ? Sv per Bq h m-3. The corresponding equilibrium equivalent dose
rates to organs are given in the accompanying electronic disk. The equilibrium effective dosecan be expressed in terms of potential alpha energy exposure for a given F value; for F=0.4
the effective dose arising from the inhalation of 222Rn gas alone is ? mSv per WLM (? Sv per
J h m-3) and for F=0.2 effective dose is ? mSv per WLM (? Sv per J h m-3). Comparing thesenumbers with the effective doses arising from the inhalation of radon progeny shows that thedose from inhaling radon gas is only a small component; less than 10%.
(Data will be provided in the final version of this document.)
12.5.3. Ingestion of radon(723) Equivalent doses to organs per unit activity of 222Rn ingested are given in theaccompanying electronic disk. The effective dose per unit intake of ingested 222Rn is ? Sv per
Bq.
(Data will be provided in the final version of this document.)
12.5.4. Use of dose coefficients for radon-222 and radon-220 and their short lived decay
products(724) For the radioisotopes of most elements, dose coefficients are given in this reportseries for different exposure conditions (mainly different chemical forms) with the advice thatin situations where more specific data are available, and estimated doses warrant moredetailed consideration, site specific dose coefficients may be calculated.
(725) Radioisotopes of radon represent a special case since there is substantial direct
evidence of lung cancer induction resulting from inhalation of 222Rn and its radioactive
progeny (ICRP, 2000). Epidemiological data clearly show that tobacco smoke is a more
powerful lung carcinogen that accounts for many more lung cancer cases than radon
inhalation (ICRP, 2010). Background lung cancer rates in different populations will differ
according to smoking prevalence and will change with time as habits change. In transportingrisk estimates for radiation induced cancer across populations and calculating overall andrelative detriment values, ICRP does not take account of smoking statistics. Thus, it should berecognised that ICRP nominal risk coefficients and dose coefficients apply to a mixed
population of smokers and non-smokers.
(726) Dose coefficients are given in this publication for the inhalation of radon isotopes
and their progeny in two situations of exposure:- Indoor Workplaces and Mines. The value
for Indoor Workplaces should also be applied to other situations of exposure, including thosein tourist caves, water supply facilities and spas. The task group calculated similar dosecoefficients for indoor workplaces, tourist caves, water supply facilities and spas. In
238

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9434
9435
9436
9437
9438
9439
9440
9441
9442
9443
9444
9445
9446
9447
9448
9449
9450
9451
9452
9453
9454
9455
9456
9457
9458
9459
9460
9461
9462
9463
9464
9465
9466
9467
9468
9469
9470
9471
9472
9473
9474
9475
9476
9477
9478
9479
9480
9481
9482
9483
9484

circumstances of occupational exposure to radon and progeny which require the applicationof the system of protection and the calculation of worker doses, it is envisaged that theappropriate reference dose coefficient will be applied. Employers may also wish to makeassessments of risk to their workers. It would then be appropriate to take account of thespecific conditions of exposure (aerosol characteristics, equivalent factors, etc) in thecalculation of lung dose, and of the individual characteristics of workers, including smoking
habits, in estimating the associated risks.
References
AGIR (Advisory Group on Ionising Radiation) (2009). Radon and public health. Doc HPA, RCE-11,
ISBN 978-0-85951-644-0. Available at www.hpa.org.uk.
Andersson, I. O.; Nilsson, I. (1964). Exposure following ingestion of water containing radon-222. In:
IAEA Symposium on Assessment of Radioactivity in Man: Vienna, IAEA, pp. 317-326.
Becker, H. K., Reineking, A., Scheibel, H. G. and Porstendörfer, J. (1984). Radon daughter activity
size distributions. Radiat. Prot. Dosim., 7(1-4), 147-150.
Bell, C. M. J.; Leach, M. O. (1982). A compartmental model for the investigation of the influence ofphysiological factors on the rate of Xe-133 and Ar-37 from the body. Phys. Med. Biol.
27:1105–1117.
Bernard, S. R.; Snyder, W. S. (1975). Metabolic models for estimation of internal radiation exposure
received by human subjects from inhalation of noble gases. ORNL Report 5046, pp. 197204.
Bigu, J. and Kirk, B. (1980). Determination of the unattached radon daughter fractions in someuranium mines.
Presented at the workshop on attachment of radon daughters,
measurements techniques and related topics, October 30, 1980, University of Toronto.
(Report available from CANMET, P.O. Box 100, Elliot Lake, Ontario, Canada).
Boulaud, D., & Chouard, J. C. (1992). Submicron sized aerosol and radon progeny measurements ina uranium mine. Radiat. Prot. Dosim., 45(1-4), 91-94.
Brown, W. L.; Hess, C. T. (1992). Measurement of the biotransfer and time constant of radon fromingested water by human breath analysis. Health Phys. 62:162-170.
Busgin, A., van der Vooren, A., & Phillips, C. R. (1981). Measurements of the total and radioactive
aerosol size distribution in a Canadian uranium mine. American Industrial Hygiene
Association Journal, 42, 310-314.
Butterweck, G., Porstendörfer, J., Reineking A. and Kesten J. (1992). Unattached Fraction and the
Aerosol Size Distribution of the Radon Progeny in a Natural Cave and Mine Atmospheres.
Radiat. Prot. Dosim., 45(1-4), 167-170.
Cavallo, (1997). Understanding aerosols in uranium mines in order to compute the lung dose for
uranium miners. J. of Aerosol Sci., 28, Suppl. 1, S435- S436.
Cavallo, (2000). Understanding mine aerosols for radon risk assessment. J. Environ. Radioactivity
51, 99-119.
Cavallo, A. J. (1998). Reanalysis of 1973 activity-weight particle size distribution measurements inactive US uranium mines. Aerosol Science and Technology, 29, 31-38.
Cavallo, A., Hutter, A., Shebell, P. (1999). Radon progeny unattached fraction in an atmosphere far
from radioactive equilibrium. Health Physics, 76 (5), pp. 532-536.
Charles, M. W. (2004). The skin in radiological protection ─ recent advances and residual
unresolved issues. Radiat. Prot. Dos., 109(4), 323-330.
Chen, R. T., Cheng, Y.-S., Hopke, P. K., Tung, C.-J. and Pourprix, M. (1997). Electrical mobility andsize distribution of aged 212Pb nanometer carriers in nitrogen gas. J. Aeerosol Sci. Vol.
28(8), 1465-1477.
Chen C.-J., Liu C.-C., Lin Y.-M. (1998). Measurement of equilibrium factor and unattached fractionof radon progeny in Kaohsiung, Taiwan. Appl. Radiat. Issot. 49(12) 1613-1618.

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DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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9486
9487
9488
9489
9490
9491
9492
9493
9494
9495
9496
9497
9498
9499
9500
9501
9502
9503
9504
9505
9506
9507
9508
9509
9510
9511
9512
9513
9514
9515
9516
9517
9518
9519
9520
9521
9522
9523
9524
9525
9526
9527
9528
9529
9530
9531
9532
9533
9534
9535
9536

Cheng, Y.-S., Chen, T.-R., Wasiolek, P. T., Van Engen, A. (1997). Radon and radon progeny in theCarlsbad caverns. Aerosol Science and Technology, 26, 74-92.
Cheng, Y.-S., Chen, R. T., Yeh, H. C., Bigu, J, Holub, R., Tu, K., Knutson, E. O. and Falk, R. (2000).
Intercomparison of activity size distribution of thoron progeny and a mixture of radon andthoron progeny. J. Environ. Radioactivity 51, 59-78.
Conn, H. L. (1961). Equilibrium distribution of radioxenon in tissue: Xenon-hemoglobin association
curve. J. Appl. Physiol. 16:153-157.
Cooper, J. A., Jackson, P. O., Langford, J.C., Petersen, M. R., and Stuart, B. O. (1973).
Characteristics of attached radon-222 daughters under both laboratory and field conditions
with particular emphasis on the underground uranium mine environment. Report to the U.S.
Bureau of Mines; Contract Report H0220029, Battelle Pacific Northwest Laboratories.
Correia, J.; Weise, S.; Callahan, R.; Strauss, H. (1987). The Kinetics of ingested Rn-222 in humans
determined from measurements with Xe-133 (Boston: Massachusetts General Hospital).
Crawford, D. J. (1980). Radiological characteristics of 219Rn. Health Physics, 39, 449-461.
Crawford-Brown, D. J. (1989). The biokinetics and dosimetry of radon-222 in the human bodyfollowing ingestion of groundwater. Environ. Geochem. Health 11:10-17.
Dundulis, W. P.; Bell, W. J.; Keene, B. E.; Dostie, P. J. (1984). Radon-222 in the gastrointestinal
tract: A proposed modification of the ICRP Publication 30 model. Health Phys. 47:243–
252.
Eatough, J. P., Henshaw, D. L. (1992). Radon and thoron associated dose to the basal layer of theskin. Phys. Med. Biol. 37, 955-67.
El-Hussein, A. (2005). A study on natural radiation exposure in different realistic living rooms.
Journal of Environmental Radioactivity 79 355-367.
El-Hussein, A., Ahmed, A. and Mohammed, A. (1998). Radiation dose to the Human Respiratory
Tract from inhalation of radon-222 and its progeny. Appl. Radiat. Isot. Vol. 49, No. 7, pp.
783-790.
Ellis, K. J.; Cohn, S. H.; Susskind, H.; Atkins, H. L. (1977). Kinetics of inhaled krypton in man.
Health Phys. 33:515-522.
Fernau, A.; Smereker, H. (1933). Concerning the remaining radioactive substance in organisms due toradon emanation. Strahlentherapie 46:365-373.
George, A. C., Hinchliffe, L., and Sladowski, R. (1975). Size distribution of radon daughters inuranium mine atmospheres. American Industrial Hygeine Association Journal, 36, 484.
Geranios, A. Nikolopoulos, D., Louizi, A, et al., 2004. Multiple radon survey in spa of Loutra
Edipsou (Greece). Radiat. Prot. Dosim. 112(2), 251-258.
Gosink, T. A.; Baskaran, M.; Holleman D. F. (1990). Radon in the human body from drinking water.
Health Phys. 59: 919-924.
Harley, J. H.; Jetter, E.; Nelson, N. (1951). Elimination of radon from the body. New York, NY: U.S.
Atomic Energy Commission, New York Operations Office; Report No. 3. Reissued as
Health and Safety Report, HASL-32 (1958). New York: U.S. Atomic Energy Commission.
New York Operations Office. Also see: Harley, J. H.; Jetter, E.; Nelson, N. (1994).
Elimination of radon from the body. Environmental International 20:573-584.
Harley, N. H., Robbins E. S. (1992). 222Rn alpha dose to organs other than the lung. Radiat. Prot.
Dosim. 45, 617-622.
Harley, N. H.; Robbins, E. S. (1994). A biokinetic model for 222Rn gas distribution and alpha dosein humans following ingestion. Environ. Int. 20:605-610.
Hattori, T. and Ishida, K. (1994). Equilibrium factor and unattached fraction of radon in nuclear
power plants. Radiat. Prot. Dosim., 55(3), 191-197.
Hattori, T. Ichiji, T., and Ishida, K. (1995). Behaviour of radon and its progeny in a Japanese office.
Radiat. Prot. Dosim., 62(3), 151-155.
Hopke, P., Jenson, B., Li, C. S., Montassier, N. Wassiolek, P., Cavallo, A. J., Gatsby K. Scocolow, R.
H. and James, A. C. (1995). Assessment of the exposure to and dose from radon decay
products in normally occupied homes. Environ. Sci. Technol. 29: 1359-1364 (1995).

240

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9537
9538
9539
9540
9541
9542
9543
9544
9545
9546
9547
9548
9549
9550
9551
9552
9553
9554
9555
9556
9557
9558
9559
9560
9561
9562
9563
9564
9565
9566
9567
9568
9569
9570
9571
9572
9573
9574
9575
9576
9577
9578
9579
9580
9581
9582
9583
9584
9585
9586
9587
9588

Huet, C. Tymen, G., Boulaud, D., (2001a). Long-term measurements of equilibrium factor andunattached fraction of short-lived radon decay products in dwelling – comparison withPraddo Model. Aerosol Science and Technology 35, 553-563.
Huet, C. Tymen, G., Boulaud, D., (2001b). Size distribution, equilibrium ratio and unattachedfraction of radon decay products under typical indoor domestic conditions. The Science of
the Total Environment, 272, 97-103.
Hursh, J. B.; Morken, A.; Thomas, P. D.; Lovaas, A. (1965). The fate of radon ingested by man.
Health Phys. 11:465-476.
ICRP (1975). International Commission on Radiological Protection, Report of the Task Group on
Reference Man, ICRP Publication 23. Oxford: Pergamon Press.
ICRP (1993). Protection against radon-222 at home and at work. ICRP Publication 65. Annals of the
ICRP 23(2), Pergamon Press, Oxford.
ICRP (1994a). Human respiratory tract model for radiological protection. ICRP Publication 66.
Annals of the ICRP, 24(1-3), Pergamon Press, Oxford.
ICRP (1994b). Dose coefficients for intakes of radionuclides by workers. ICRP Publication 68.
Annals of the ICRP, 24(4), Pergamon Press, Oxford.
ICRP (2002). International Commission on Radiological Protection. Basic anatomical andphysiological data for use in radiological protection: Reference values. ICRP Pub. 89. Ann.
ICRP, 32(3-4). Oxford: Pergamon Press.
ICRP (2006). International Commission on Radiological Protection. Human Alimentary Tract Modelfor Radiological Protection. ICRP Publication 100. Ann. ICRP, 26(1-2). Oxford:
Pergamon Press.
Iimoto, T. (2000). Time variation of the radon equilibrium factor in reinforced concrete dwelling.
Radiat. Prot. Dosim., 92(4), 319-321
Iimoto, T., Kosako, T. and Sugiura, N. (2001). Measurements of summer radon and its progeny
concentrations along with environmental gamma dose rates in Taiwan. Journal ofEnvironmental Radioactivity, 57 (1), 57-66
Iyogi, T., Ueda, S., Hisamatsu, S., Kondo, K., Sakurai, N. and Inaba, J. Radon concentrations inindoor occupational environments in Aomori Prefecture, Japan. (2003). Journal ofEnvironmental Radioactivity 67, 91-108.
James, A C, Strong, J C, Cliff, K D, and Stranden. (1988). The significance of equilibrium andattachment in radon daughter dosimetry. Radiat. Prot. Dosim., 24, 451-455.
Kahn, A., Bandi, F., Gleasur, R.W., Phillips, C.R., & Duport, P. (1987). Underground measurementsof aerosol and activity distributions of radon and thoron progeny. P.K. Hopke, Radon andits decay products Washington, DC: (p. 219), The American Chemical Society.
Kety, S. G. (1951). The theory and applications of the exchange of inert gases at lung and tissue.
Pharmacol. Rev. 3:1-41.
Khursheed, A. (2000). Doses to systemic tissues from radon gas. Radiat. Prot. Dosim. 88:171-181.
Kirk, W. P.; Parish, P. W; Morken, D. A. (1975); In vivo solubility of Kr-85 in guinea pig tissues.
Health Physics 28, 249-261 (1975).
Knutson, E. O., and George, A. C. (1990). Reanalysis of the data on the particle size distribution ofradon progeny in uranium mines. Proceedings of the 29th life sciences symposium, indoor
radon and lung cancer: reality or myth? October 16-19, Part 1. Edited by F. T. Cross.
Pacific Northwest Laboratories Richland, WA (p. 149).
Kojima, H. and Abe, S. (1988). Measurements of the total and unattached radon daughters in ahouse. Radiat. Prot. Dosim., 24(1/4), 241- 244.
Kranrod, C., Tokonami, S., Ishikawa, T., Sorimachi, A., Janik, M., Shigaki, R., Furukawa, M.,
Chanyotha, S. and Chankow, N. (2009). Mitgation of the effective dose of radon decay
products through the use of an air cleaner in a dwelling in Okinawa, Japan. Applied
Radiation and Isotopes 67(6), 1127-1132.
Labidi, S., Al-Azmi, D., Mahjoubi, H., Ben Salah, R. (2010). Radon in elementary schools in
Tunisia. Radiopotection, 45(2), 209-217.

241

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9589
9590
9591
9592
9593
9594
9595
9596
9597
9598
9599
9600
9601
9602
9603
9604
9605
9606
9607
9608
9609
9610
9611
9612
9613
9614
9615
9616
9617
9618
9619
9620
9621
9622
9623
9624
9625
9626
9627
9628
9629
9630
9631
9632
9633
9634
9635
9636
9637
9638
9639
9640

Leggett, R. W.; Williams, L. R. (1995). A proposed blood circulation model for reference man.
Health Phys. 69:187-201.
Lettner, H., Hubmer, A.K., Rolle, R., Steinhäusler, F. (1996). Occupational exposure to radon intreatment facilities of the radon-spa Badgastein, Austria. Environ. Intern 22 (1), S399S407.
Maged, A. F. (2006). Radon concentrations in elementary schools in Kuwait. Health Phys. 90(3),258-262.
Marsh J W and Birchall A (1998). Sensitivity analysis of the weighted equivalent lung dose per unit
exposure from radon progeny. NRPB-M929 Health Protection Agency, Chilton, Didcot,
Oxon, OX11 ORQ, UK.
Marsh, J. W., Bessa, Y., Birchall, A., Blanchardon, E., Hofmann, W., Nosske. D. and L. Tomasek(2008). Dosimetric models used in the Alpha-Risk project to quantify exposure of uranium
miners to radon gas and its progeny. Radiat. Prot. Dosim., 130(1) 101-106.
Marsh, J.W., Birchall, A., Butterweck, G., Dorrian, M.-D., Huet, C., Ortega, X., Reineking, A.,
Tymen, G., Schuler, Ch., Vargas, A., Vezzu, G. and Wendt. J. (2002). Uncertainty
analysis of the weighted equivalent lung dose per unit exposure to radon progeny in thehome. Radiat. Prot. Dosim., 102(3), 229-248.
Meyer, S. (1937). Physical foundations of radon cures. Strahlentherapie. 58:656-663.
Misdaq, M. A. and Amghar, A. (2005). Radon and thoron emanation from various marble materials:
impact on the workers. Radiation Measurements 39, 421-430.
Misdaq, M. A. and Flata, K. (2003). The influence of the cigarette smoke pollution and ventilation
rate on alpha activities per unit volume due to radon and its progeny. Journal ofEnvironmental Radioactivity, 67, 207-218.
Mohammed, A. (1999). Activity size distributions of short-lived radon progeny in indoor air. Radiat.
Prot. Dosim., 86(2), 139-145.
Mohammed, A. (2005). Study on radon and radon progeny in some living rooms. Radiat. Prot.
Dosim., 117(4), 402-407.
NAS (1999). Risk assessment of radon in drinking water. National Research Council. National
Academy of Sciences. Washington, D.C.: National Academy Press.
National Research Council, (1991). Comparative Dosimetry of Radon in Mines and Homes.
National Academy Press (Washington, DC). ISBN 0-309-04484-7 (1991).
Nickell, W.B. (2005). Skelton J Breast fat and fallacies: more than 100 years of anatomical fantasy.
Journal of Human Lactation, 21(2):126-130
NRC (National Research Council), (1999). Health effects of exposure to radon. Washinghton, DC:
National Academy Press; BEIR VI, ISBN: 0-309-05645-4.
Nussbaum, E. and Hursh, J. B. (1958). Radon solubility in fatty acids and triglycerides. J Phys.
Chem. 62, 81-84.
Nussbaum, E.; Hursh, J. B. (1957). Radon solubility in rat tissues. Science 125:552.
Olfert, J. S., Symonds, J. P. R. and Collings, N. (2007). The effective density and fractal dimensionsof particles emitted from a light-duty vehicle with a diesel oxidation catalyst. Aerosol
Science 38 69-82.
Park, K., Cao, F., Kittelson, D. B. and McMurry, P. H. (2003). Relationship between particle massand mobility for diesel exhaust particles. Environ. Sci. Technol. 37, 577-583.
Peterman, B. F.; Perkins C. J. (1988). Dynamics of radioactive chemically inert gases in the humanbody. Radiat. Prot. Dosim. 22:5–12.
Porstendörfer, J (1994). Tutorial/Review: Properties and behaviour of radon and thoron and theirdecay products in the air. J. Aerosol Sci., 25(2), 219-263.
Porstendörfer, J (1996). Radon: Measurements related to dose. Environmental International, Vol.
22, Suppl. 1, pp. S563-S583.
Porstendörfer, J (2001). Physical parameters and dose factors of the radon and thoron decay
products. Radiat. Prot. Dosim., 94(4), 365-373.
Porstendörfer, J., Pagelkopf, P. and Gründel, M. (2005). Fraction of the positive 218Po and 214Pb

242

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9641
9642
9643
9644
9645
9646
9647
9648
9649
9650
9651
9652
9653
9654
9655
9656
9657
9658
9659
9660
9661
9662
9663
9664
9665
9666
9667
9668
9669
9670
9671
9672
9673
9674
9675
9676
9677
9678
9679
9680
9681
9682
9683
9684
9685
9686
9687
9688
9689
9690

clusters in indoor air. Radiat. Prot. Dosim., 113(3), 242-351.
Porstendörfer, J. and Reineking, A. (1999). Radon: Characteristics in air and dose conversion
factors. Health Phys. 76(3), 300-305.
Ramachandran, T.V. and Subba Ramu, M.C. (1994). Variation of equilibrium factor F between
radon and its short-lived decay products in an indoor atmosphere.
NuclearGeophysics, 8 (5), pp. 499-503.
Ramsay, D. T. ; Kent, J. C.; Hartmann, R. A. ; Hartmann, P. E. (2005). Anatomy of the lactating
human breast redefined with ultrasound imaging. J. Anat. 206:525–534.
Reichelt, A., Lehmann, K.H., Reineking, A., Porstendörfer, J., Schwedt, J. and Streil, T. (2000).
Radon at workplaces. In: Proc. IRPA-10, Hiroshima, Japan, 14-19 May (2000).
Reineking, A., Butterweck, G., Kesten, J. and Porstendörfer J (1992). Thoron gas concentration andaerosol characteristics of thoron decay products. Radiat. Prot. Dosim., 45(1/4), 353-356.
Reineking A, Knutson E A, George A C, Solomon S B, Kesten J, Butterweck G and Porstendorfer J(1994). Size distribution of unattached and aerosol-attached short-lived radon decay
products: some results of intercomparison measurements. Radiat. Prot. Dosim., 56(1-4),
113-118.
Reineking, A and Porstendörfer, J. (1990). “Unattached” fraction of short-lived Rn decay products inindoor and outdoor environments: an improved single-screen method and results. Health
Physics, 58(6) 715-727.
Richardson, R. B.; Eatough, J. P.; Henshaw, D. L. (1991). Dose to red bone marrow from naturalradon and thoron exposure. Br. J. Radiol. 64:608-624.
Rosvenská, K., Thinová, L., Ždímal, V. (2008). Assessment of the dose from radon and its decay
products in the Bozkov dolomite cave. Radiat. Prot. Dosim., 130(1), 34-37.
Ruzer, L. S., Nero A.V. and Harley N. H. (1995). Assessment of lung deposition and breathing rateof underground miners in Tadijikistan. Radiat. Prot. Dosim., 58, 261-268.
Sainz, C., Quidós, L. S., Fuente, I., Nicolás, J., Quidós, L. (2007). Analysis of the main factors
affecting the evaluation of the radon dose in workplaces: The case of the tourist caves.
Journal of Hazardous Materials, 145, 368-371.
Sharma, N.; Hess, C. T.; Thrall, K. D. (1997). A compartment model of water radon contamination in
the human body. Health Phys. 72:261-268.
Sinclair, D., Countess, R. J. and Hoopes, G. S (1974). Effect of relative humidity on the size of
atmospheric aerosols particles. Atmos. Environ., 8, 1111-1117.
Solomon, S. B., Cooper, M. B., O’Brien, R. S., Wilkinson, L., (1992). Radon exposure in alimestone cave. Radiat. Prot. Dosim., 45(1-4), 171-174.
Solomon, S. B., Wilks, M., O’Brien, R. S. and Ganakas, G. (1993). Particle sizing of airborne
radioactivity field measurements at Olympic Dam. Report ARL/TR113. ISSN 0157-1400.
Australian Radiation Laboratory, Lower Plenty Road, Yallambie VIC 3085.
Solomon, S. B., O’Brien, R. S., Wilks, M. and James, A. C. (1994) Application of the ICRP’s new
respiratory tract model to an underground uranium mine. Radiat. Prot. Dosim., 53(1-4),
261-268.
Soto, J., Gómez, J. (1999). Occupational doses from radon in Spanish spas. Health Phys. 76(4),398-401.
Suomela, M.; Kahlos, H. (1972). Studies on the elimination rate and the radiation exposure following
ingestion of Rn-222 rich water. Health Phys. 23:641-652.
Susskind, H.; Atkins, H. L.; Cohn, S. H.; Ellis, K. J.; Richards, P. (1977). Whole-body retention ofradioxenon. J. Nucl. Med. 18:462-471.
Tokonami, S., Fukutsu, K., Yamada, Y., Yatabe, Y. (2005). Particle size measurement of radon
decay products using MOUDI and GSA. In: High Levels of Natural Radiation and Radon
Areas: Radiation Dose and Health Effects (T. Sugahara et al., eds.). International Congress
Series 1276, 278-280, Elsevier.

243

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9691
9692
9693
9694
9695
9696
9697
9698
9699
9700
9701
9702
9703
9704
9705
9706
9707
9708
9709
9710
9711
9712
9713
9714
9715
9716
9717
9718
9719
9720
9721
9722
9723
9724
9725
9726
9727
9728
9729
9730
9731
9732
9733
9734
9735
9736
9737
9738
9739
9740
9741

Tokonami, S., Iimoto, T. and Kurosawa. (1996a). Continuous measurement of the equilibrium factor,
F and the unattached fraction, fp of radon progeny in the environment. Environmental
International, 22, Suppl. 1, S611-S616.
Tokonami, S., Matsumoto, M. Furukawa, M., Fujimoto, K., Fujitaka, K., and Kurosawa, R. (1996b).
Behavior of radon and its progeny at working place. In: Proc. IRPA-9.
Trautmannsheimer, M., Schindlmeier, W., Börner, K. (2003). Radon concentration measurements andpersonnel exposure levels in Bavarian water supply facilities. Health Phys. 84(1), 100-110.
Tschiersch, J., Li, W. B. and Meisenberge, O. (2007) Increased indoor thoron concentrations andimplication to inhalation dosimetry. Radiat. Prot. Dosim., 127(1-4), 73-78.
Tu K W and Knutson E O. (1988) Indoor radon progeny particle size distribution measurements
made with two different methods. . Radiat. Prot. Dosim., 24(1/4) 251-255.
Tu K W, Knutson E O and George A C. (1991) Indoor radon progeny aerosol size measurements inurban, surban, and rural regions. Aerosol Science and Technolgy 15 170-178.
Vanmarcke, H., Berkvens, P. and Poffijn, A. (1989) Radon versus Rn daughters. Health Physics,
56(2), 229-231.
Vargas, A., Ortega, X. and Porta, M. (2000). Dose conversion factor for radon concentration inindoor environments using a new equation for the F-fp correlation. Health Phys. 78(1): 8085.
Vaternahm, T. (1922). Comparative investigation of the radon capacity of exhaled breath after
drinking of radon ladened water and oil. Zschr. Phys. Diat. Ther. 26:361-364.
Vaupotič, J. (2007) Nano-size radon short-lived progeny aerosols in Slovenian kindergartens in
wintertime. Chemosphere, 69 (6), 856-863.
Vaupotič, J. (2008a). Nanosize radon short-lived decay products in air of the Postojna Cave. Scienceof the total environment 393 27-38.
Vaupotič, J. (2008b). Levels of nanosize radon decay products in indoor air: A comparison fordifferent environments. Coll. Antropol. 32 Suppl. 2 99-104.
Vaupotič, J. and Kobal, I (2001). Radon exposure in Slovenia spas. Radiat. Prot. Dosim. 97(3) 265270
Vaupotič, J. and Kobal, I. (2006) Effective doses in schools based on nanosize radon progeny
aerosols. Atmospheric Environment, 40 (39), 7494-7507.
Vogiannis, E. Nikolopoulos, D., Halvadakis, C. P (2004a). Contribution of 222Rn-bearing water tothe occupational exposure in thermal baths. Environmental International 30, 621-629.
Vogiannis, E., Nikolopoulos, D., Loouizi, A., Halvadakis, C. P. (2004b). Radon exposure in thethermal spas of Lesvos island—Greece. Radiat. Prot. Dos., 111(1), 121-127.
Vogiannis, E., Nikolopoulos, D., Loouizi, A., Halvadakis, C. P. (2004c). Radon variations during
treatment in thermal spas of Lesvos Island (Greece). J. Environ. Radioactivity., 76, 283294.
von Döbeln, W.; Lindell, B. (1964). Some aspects of radon contamination following ingestion. Arkiv
für Fysik 27:531-572.
Weingartner, E., Burtscher, H. and Baltensperger, U. (1997) Hygroscopic properties of carbon anddiesel soot particles. Atmospheric Environ. 31 2311-2327.
Wilkening, M. H., Romero, V. (19781). 222Rn and atmospheric electrical parameters in the Carlsbad
caverns. J. Geophys. Res. 86:9911-9916.
Wu-Tu, K., Fisenne, I. M. and Hutter, A. R. (1997). Short - and long-lived radionuclide particle size
measurements in a uranium mine. Report EML-588, Environmental Measurements
Laboratory, U.S. [www.eml.doe.gov/publications/reports/eml588.pdf]
Yu, D.; Kim, J. K. (2004). A physiologically based assessment of human exposure to radon released
from groundwater. Chemospher 54:639-645.
Yu, K. N., Cheung, T., Guan, Z. J., Mui, B. W. N. and Ng, Y. T. (2000). 222Rn, 220Rn and theirprogeny concentrations in offices in Hong Kong. Journal of Environmental Radioactivity
48 211 – 221.

244

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
9742
9743
9744
9745
9746
9747
9748

Yu, K. N., Young, M. C. E. and Li, K. C. (1996). A survey of radon properties for dwellings forHong Kong. Radiat. Prot. Dosim., 63(1) 55-62.
Yu, K. N., Young, M. C. E., Stokes, M. J. and Tang, K. K. (1998). Radon properties in offices.
Health Phys. 75(2) 159-164.
Zhang, L. Guo, Q. and Zhuo, W. (2010). Measurement of the 212Pb particle size distribution indoors.
Radiat. Prot. Dosim., 141(4), 371-373.

245

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9752
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13.
13.1.

Chemical Forms in the Workplace(727) Radium is an alkaline earth element, which mainly occurs in oxidation states II. It isa chemical analogue of calcium. Chemical and physical forms encountered in industry include
oxides, nitrates, chlorides, sulphates, and luminising residues. Radium can be found in trace
amounts in uranium ores. A mixture of radium and beryllium is used as a neutron source.
224
Ra, 226Ra and 228Ra are the most common isotopes of radium. 223Ra is currently underinvestigation for use in medicine as a treatment for bone metastases.
Table 13-1. Isotopes of radium addressed in this report
Isotope
Ra-223
Ra-224Ra-225
Ra-226aRa-227
Ra-228aRa-230

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9781
9782
9783
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9789

Radium (Z = 88)

a

13.2.

Physical half-life
11.43 d3.66 d
14.9 d1600 y42.2 m
5.75 y93 m

Decay mode
A
A
BA
BBB-

Data for these radionuclides are given in the printed copy of this report. Data for other radionuclides
are given on accompanying electronic disk.

Routes of Intake

13.2.1. Inhalation
Absorption Types and parameter values(728) Several studies have been reported on the behaviour of inhaled radium in man
following accidental intakes, especially of the sulphate, which was used in powder form in
gamma-ray sources. However, it is difficult to estimate the contribution of absorption to lungclearance in such cases, because the systemic excretion of radium is predominantly by the
faecal route. Information is available from experimental studies of radium as nitrate, or in fly
ash.
(729) Absorption parameter values and Types, and associated fA values for particulate
forms of radium are given in Table 13-2.
Radium nitrate (Ra(NO3)2)(730) Following administration of 232UO2(NO3) with its decay products to rats byintratracheal instillation (Ballou et al., 1986), about 3% of the 224Ra present was retained in
the lung after 1 day, consistent with assignment to Type F. (For further information see theuranium inhalation section.)(731) Following administration of Ra(NO3)2 (alone or with thorium nitrate) to rats byintratracheal instillation (Moody and Stradling 1992; Moody et al., 1994), about 14% of theinitial lung deposit (ILD) was retained in the lung after 6 hours and ~5% ILD after 1 or 7
days. From the results, it was assessed here that fr was about 0.95 and sr about 10 d–1, but it
was not possible to estimate ss.
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9791
9792
9793
9794
9795
9796
9797
9798
9799
9800
9801
9802
9803
9804
9805
9806
9807
9808
9809
9810
9811
9812
9813
9814
9815
9816
9817
9818
9819
9820
9821
9822
9823
9824
9825
9826
9827
9828
9829
9830
9831
9832
9833
9834
9835
9836
9837

(732) Based on the results of the experiments outlined above, specific absorption
parameter values for radium nitrate were estimated here to be: fr = 1 and sr = 10 d-1 (consistent
with assignment to default Type F). However, although specific parameter values for radium
nitrate based on in vivo data are available, they are not adopted here, because inhalation
exposure to it is unlikely. Instead, radium nitrate is assigned to Type F. However, the data
are used as the basis for the default rapid dissolution rate for radium. Hence specificparameter values for radium nitrate would be the same as default Type F radium parametervalues.
Radium sulphate (RaSO4)(733) Marinelli et al. (1953) reported measurements on six people following accidental
inhalation of a mixture of radium and barium sulphates, resulting from rupture of a capsule.
The observed lung retention half-time of 120 d suggested that the material was relatively
insoluble. Looney and Archer (1956) reported measurements on two men, also following theinhalation of a mixture of radium and barium sulphates from a damaged source. The resultsfrom both studies are difficult to interpret.
Coal fly ash(734) Kalkwarf et al. (1984) measured the in vitro dissolution of radionuclides in 11
samples of coal fly ash (3–5 size fractions from three sources). Less than 0.2% of the 226Ra
present dissolved during the 60 days, indicating Type S behaviour.
Uranium ore dust
(735) Duport et al. (1991) measured the dissolution in simulated lung fluid of long lived
radionuclides in uranium ore dust from Canadian mines. (For further information see theuranium section relating to uranium ore dust and to decay products of uranium formed in the
respiratory tract). For high grade ore, measurements were made for up to 60 days. Results
were presented as undissolved fractions as functions of time, and showed two components,
which were expressed as Class D (rapid) and Class Y (slow) fractions. For 226Ra the rapidly
dissolved fraction was 0.12. HRTM parameter values fitted to the 210Pb data by Marsh et al.
(2011) were: fr = 0.11, sr = 7.3 d–1 and ss = 0.0004 d–1, indicating assignment to Type M. For
226
Ra, no effects of size were observed in total dissolution over 40 days for particles in size
ranges 7–10, 3–7, 1–3 and <1 µm. For low grade and medium grade ores, measurements weremade for 12 days, but only on samples of relatively coarse dust, the smallest fraction being<37 µm. For 226Ra, rapidly dissolved fractions were lower, 0.07, indicating assignment toType S.
Other compounds(736) In another case of human inhalation, Toohey et al. (1984) reported a lung retention
half-time of 120 d. However, the radium compound was unknown, (Ra-contaminated dust
from grinding old rubber liners from ion-exchange tanks). It was considered by the authors to
be insoluble, because the amount recovered in fecal excretion corresponded closely to theamount clearing from the lungs.
Decay products of radium formed in the respiratory tract(737) The general approach to treatment of decay products formed in the respiratory tract
is described in Part 1, Section 3.2.3. In summary, it is expected that generally the rate at
which a particle dissociates is determined by its matrix, and hence the physico-chemical form
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9845
9846
9847
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9850
9851
9852
9853
9854
9855
9856
9857
9858
9859
9860
9861
9862
9863
9864
9865
9866
9867
9868
9869
9870
9871
9872
9873
9874
9875
9876
9877
9878
9879
9880
9881
9882
9883
9884
9885

of the inhaled material. It is recognised that nuclei formed by alpha decay within a particle
matrix may be expelled from it into the surrounding medium by recoil, but to implement thisroutinely would add greatly to the complexity of calculations. It is expected that the behaviourof soluble (e.g. Type F) material in the respiratory tract would depend on its elemental form,
i.e. that of the decay product. Nevertheless, for simplicity, in this series of documents theabsorption parameter values of the parent are, by default, applied to all members of the decay
chain formed in the respiratory tract. Exceptions are made for noble gases formed as decay
products, which are assumed to escape from the body directly, in addition to other routes ofremoval. For calculation purposes it is assumed that radon formed as a decay product within
the respiratory tract escapes from the body at a rate of 100 d–1, in addition to other routes ofremoval. (For further information see Part 1, Section 3.2.3, and the section on decay productsof thorium formed in the respiratory tract.
(738) For decay schemes of radium isotopes in the natural decay series, including 223Ra,
224
Ra, 226Ra and 228Ra, see the uranium and thorium sections.
(739) Studies specifically comparing the behaviour of radium with that of its decay
products (lead, bismuth and thallium isotopes) are summarised here. For further informationon these elements, see the lead and bismuth inhalation sections.
(740) Studies relating to the loss from the body (emanation) of radon formed in the lungs
are summarised in the section on decay products of thorium formed in the respiratory tract,even though radium is its immediate predecessor. It was considered useful to have therelevant information in one place, and to avoid repetition. The most important practicalapplication of radon emanation is measurement of exhaled 220Rn to assess intakes ofrelatively insoluble thorium (thoron-in-breath measurements) and most studies investigatingradon formed in the respiratory tract involved thorium deposited in the lungs.
(741) Ballou et al. (1986) measured lung retention and tissue distribution of 232U, 228Th,
224
Ra, 212Pb, 212Bi and 208Tl at 24 hours after intratracheal instillation into rats of 232U nitratewith its decay products. (For further information, see the uranium inhalation section.) As
noted above, for 224Ra, ~3% ILD was retained in the lungs at 24 hours. For the firstdescendant measured, 212Pb, ~2.1% ILD was measured in the lungs: correcting for thephysical decay of 212Pb gives retention of 10% ILD at 24 hours. However, measurements of212
Pb are difficult to interpret, being partly of material administered with the parent 224Ra, andpartly formed from its decay in the lungs. Furthermore, the 212Pb measured could have been
higher than that present in vivo because of ingrowth of 212Pb between dissection andmeasurement. If not due to ingrowth, the greater fractional retention of lead could reflect its
slower absorption than that of radium observed when administered separately.
(742) As described in the lead inhalation section, measurements have been made of thetissue distributions of 212Pb and its decay products, 212Bi and 208Tl, following administration
to rats of 228Th in various chemical forms (nitrate, hydroxide, fluoride, dioxide) in
equilibrium with its decay products. These included 224Ra, but it was not measured. In allthese studies the distributions of 212Bi and 208Tl were similar to each other and those of theparent 212Pb. In the study of thorium nitrate (Moody et al., 1994; Moody and Stradling, 1992)
a complementary study was carried out with 226Ra (see radium nitrate above). For 212Pb, on
average 8.4% ILD was measured in the lungs at 6 hours and 1.2% ILD at 1 day (clearance
was much faster than that of the 228Th). Correcting for the physical decay of 212Pb gives
retention of 12.5% ILD at 6 hours and 5.6% ILD at one day. This is similar to that found for226
Ra (see above), suggesting similar overall clearance of radium and lead over this period.
Rapid dissolution rate for radium
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9893
9894
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(743) From the results of studies with radium nitrate outlined above, the value of sr wasassessed to be about 10 d–1, which is applied here to all Type F forms of radium.
Extent of binding of radium to the respiratory tract(744) Evidence from the radium nitrate studies outlined above suggests that there is
probably little binding of radium. It is therefore assumed that for radium the bound state canbe neglected, i.e. fb = 0.0.
Table 13-2. Absorption parameter values for inhaled and ingested radium
Absorption parameter valuesa
Inhaled particulate materials
Default parameter valuesb,cAbsorption
Assigned forms
TypeF
NitrateM
All unspecified formsd
S—frsr (d–1)

ss (d–1)

Absorption
fromthealimentarytract, fA

1
0.2
0.01

10
3
3

–
0.005
0.0001

0.2
0.04
0.002

Ingested materials
All forms
9896
9897
9898
9899
9900
9901
9902
9903
9904
9905
9906
9907
9908
9909
9910
9911
9912
9913
9914
9915
9916
9917
9918
9919
9920
9921
9922
9923

0.2

a

It is assumed that for radium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F formsof radium (10 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
bMaterials (e.g. radium nitrate) are generally listed here where there is sufficient information to assign to adefault absorption Type, but not to give specific parameter values (see text).
c
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the (rounded) product of fr for theabsorption Type (or specific value where given) and the fA value for ingested soluble forms of radium (0.2).
dDefault Type M is recommended for use in the absence of specific information, i.e. if the form is unknown,or if the form is known but there is no information available on the absorption of that form from therespiratory tract.

13.2.2. Ingestion(745) Radium is a good chemical analogue of barium and calcium, and its absorption
depends on its chemical form. Factors affecting absorption of radium are various. It seems
that ageing significantly decreases radium absorption by a factor of 2 to 4 compared to adults(Taylor et al., 1962), whereas fasting and low calcium intake increases its absorption (Taylor
et al., 1962, Della Rosa et al., 1967).
(746) Data from balance studies reviewed by the ICRP Task Group on Alkaline Earth
Metabolism in Adult Man (ICRP, 1973) indicated the fraction of radium absorbed from foodor drinking water to be between 0.15 and 0.21. Results from a study of a single humanvolunteer who ingested a known quantity of radium suggested a higher value from 0.14 to
0.7, depending on the method of calculation (Seil et al., 1915). Normal elderly subjects
ingesting mock radium dial paint containing 224RaSO4 absorbed an average of about 0.2(Maletskos et al., 1966, 1969).
(747) In the Publication 30 (ICRP, 1979) an absorption value of 0.2 was adopted and that
was also applied to dietary intakes in Publication 67 (1993).
(748) An fA of 0.2 is used in this report for all forms of radium.

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9938
9939
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9943
9944
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9947
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9949
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9952
9953
9954
9955
9956
9957
9958
9959
9960
9961
9962
9963
9964
9965

13.2.3. Systemic Distribution, Retention and Excretion
13.2.3.1. Biokinetic database(749) The alkaline earth element radium is a physiological analogue of the alkaline earth
elements calcium, strontium, and barium but has different biokinetics from those elements
due to discrimination by biological membranes and hydroxyapatite crystals of bone. The
biokinetics of radium resembles that of barium much more closely than that of calcium orstrontium.
(750) Retention and distribution of radium have been determined in a number of persons
who were briefly exposed to radium isotopes (ICRP, 1973, 1993; Leggett, 1992). There isalso extensive information on the biokinetics of radium in laboratory animals, particularly
dogs (ICRP, 1993, Leggett, 1992). Data for human subjects and laboratory animals used in
the development of the model are summarized below in the discussion of the basis forparameter values.
13.2.3.2. Biokinetic model for systemic radium(751) The model for systemic radium applied in this report is a modification of the model
adopted in ICRP Publication 67 (1993). In the earlier version of the model the liver was
represented as a single compartment, and the kidneys were not depicted explicitly but were
included as part of Other soft tissues. In the present version the kidneys are also depicted
explicitly, and both the liver and kidneys are modelled as two compartments representing
relatively fast and relatively slow loss of radium.
(752) The structure of the present model is shown in Figure 13-1. Blood plasma (called“Blood” in Figure 13-1) is treated as a uniformly mixed pool that contains all radium inblood, exchanges activity with soft tissues and bone surfaces, and loses activity to urinary andfaecal excretion pathways. Soft tissues are divided into compartments representing twophases of loss from the liver, two phases of loss from the kidneys, and three phases of loss
from remaining soft tissues. Bone is divided into cortical and trabecular bone. Each of thesebone types is further divided into bone surfaces and bone volume. Bone volume is viewed asconsisting of two pools, one that exchanges with activity in bone surface over a period ofmonths and a second, non-exchangeable pool from which activity is removed only by bone
restructuring processes. Activity depositing in the skeleton is assigned to bone surface. Overa period of days a portion of the activity on bone surfaces moves to exchangeable bonevolume and the rest returns to plasma. Activity leaving exchangeable bone volume is divided
between bone surfaces and non-exchangeable bone volume. The assigned rate of removalfrom non-exchangeable bone volume is the reference rate of bone turnover for trabecular or
cortical bone.

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9966
9967
9968
9969
9970
9971
9972
9973
9974
9975
9976
9977
9978
9979
9980
9981
9982
9983
9984
9985
9986
9987
9988
9989
9990
9991
9992
9993
9994
9995
9996

Figure 13-1. Model for systemic radium used in this report.

Parameter values(753) Retention and distribution of radium have been determined in a number of persons
who were briefly exposed to radium isotopes (Schlundt et al., 1933; Norris et al., 1955; Mayset al., 1962, 1963; Miller and Finkel, 1965; Harrison et al., 1967; ICRP, 1973; Parks et al.,
1978; Harrison, 1981; Schlenker et al., 1982; Parks and Keane, 1983; Keane and Schlenker,
1987). These data can be supplemented with extensive biokinetic data for radium in beagles(Wood et al., 1970; Lloyd et al., 1976a,b, 1982, 1983a,b,c,d; Parks et al., 1978) and withhuman and beagle data for barium, a chemical and physiological analogue of radium. In
extrapolation of data from beagles to man, consideration must be given to the relatively low
rate of faecal excretion of heavy alkaline earths in beagles (Van Dilla et al. ,1958; Della Rosa
et al., 1967; Cuddihy and Griffith, 1972) compared with human subjects (Harrison et al.,
1967; Newton et al., 1991).
(754) Kinetic analysis of plasma disappearance curves for normal subjects intravenously
injected with radioisotopes of calcium, strontium, barium, or radium indicates that theseelements initially leave plasma at a rate of several hundred plasma volumes per day andequilibrate rapidly with an extravascular pool roughly three times the size of the plasma pool.
Total transfer rates from plasma of 70 d-1 yield reasonable fits to plasma disappearance curves
for radium and barium at times greater than 1-2 h after injection (Leggett, 1992). The rapid
early removal from plasma is not depicted in this model.
(755) Soft tissues apparently contain a substantial portion of systemic radium for a periodof days or weeks after its uptake to blood (Hursh and Lovaas, 1963; Atherton et al., 1965;
Harrison et al., 1967; Hardy et al., 1969; Schlenker et al., 1982; Qiyue et al., 1988). Based ona review of data on 226Ra in human soft tissues, Schlenker et al. (1982) estimated that softtissue retention rises to about 58% of whole body retention at 18 d after single intake and thenfalls steadily to 33% at 100 d and 6% at 1000 d. These estimates relied on assumptions andfeatures of the ICRP’s alkaline earth model introduced in the 1970s (ICRP, 1973). A modelfree fitting procedure would yield somewhat lower estimates at early times. Harrison et al.
(1967) inferred from measurements on a human subject receiving 223Ra by intravenous251

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10001
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10043
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injection that extracellular fluids of soft tissues of man contain about one-fourth ofadministered radium at 24 h. In adult beagles, soft tissues contained about 62% of the totalbody burden of intravenously injected 224Ra at 1 h, 29% at 1 d, and 12% at 7 d (Lloyd et al.,1982). The liver and kidneys contained on average about one-third of the total 226Ra in soft
tissues from 7-1190 d after its intravenous administration to adult beagles (Atherton et al.,1965).
(756) Autopsy measurements of environmental 226Ra in adult humans indicate that soft
tissues contain 10-30% of total-body 226Ra (Hursh and Lovaas, 1963; Rajewsky et al., 1965;
Maletskos et al., 1969; ICRP, 1973; Qiyue et al., 1988). These estimates have been based onmeans or pooled samples for several subjects, which may give misleading results sincemeasured 226Ra concentrations are likely to be asymmetically distributed in the population.
Using median values of 226Ra to Ca ratios obtained from the literature, Schlenker et al. (1982)
estimated that soft tissues contain 5.5-6% of the natural Ra-226 in the total body.
(757) In the present model, fractional deposition of radium in the fast-turnover soft-tissuecompartment ST0 is determined as the balance after other deposition fractions have been
assigned. As discussed below, deposition fractions of 0.25 for bone, 0.05 for intermediateterm soft tissues (ST1), 0.001 for long-term soft tissues (ST2), 0.06 for liver, 0.02 forkidneys, and 0.32 for excretion pathways are assigned to radium, leaving 0.299 for ST0. The
derived transfer rate from plasma to ST0 is 0.299 × 70 d-1 = 20.93 d-1. Based on the assumed
relative amounts of radium in ST0 and plasma, the transfer rate from ST0 to plasma is set at
one-third the transfer rate from plasma to ST0, or 6.98 d-1.
(758) The biokinetics of radium in the liver is modeled on the basis of observations of the
behavior of 224Ra and 226Ra in adult beagle dogs (Glad et al., 1960; Atherton et al., 1965;
Lloyd et al., 1982). The liver consists of compartments Liver 1 and Liver 2 with fast and slow
turnover, respectively. Radium transfers from plasma to Liver 1 and is removed from Liver 1
with a half-time of 1 d, with 99.7% returning to plasma and 0.3% moving to Liver 2. Radiumtransfers from Liver 2 to plasma with a half-time of 1 y.
(759) The biokinetics of radium in the kidneys is also based on data for adult beagle dogs
(Glad et al., 1960; Atherton et al., 1965; Lloyd et al., 1982). The kidneys are divided into
compartments Kidneys 1 and Kidneys 2 with fast and slow turnover, respectively. Radiumtransfers from plasma to Kidneys 1 and is removed from Kidneys 1 with a half-time of 8 h,with 99.7% returning to plasma and 0.3% moving to Kidneys 2. Radium transfers from
Kidneys 2 to plasma with a half-time of 1 y.
(760) The removal half-time from the long-term soft-tissue compartment ST2 to plasma isassumed to be 5 y, the same as applied in the models for calcium, strontium, and barium.
Fractional deposition of radium in ST2 is set to yield reasonable agreement with autopsy datafor persons exposed over a short period to relatively high levels of 226Ra and persons exposedover their lifetimes only to natural levels of 226Ra (Schlenker et al., 1982). It is assumed that
0.1% of radium leaving plasma enters ST2. The derived transfer rate from plasma to ST2 is0.001 × 70 d-1 = 0.07 d-1 and from ST2 to plasma is ln(2)/5 y = 0.00038 d-1.
(761) Data from human and animal studies indicate that the rate of loss of alkaline earth
elements from bone over the first few months after injection increases in the order calcium <strontium < barium < radium, and fractional long-term retention increases in the reverse
order. Some element-specific parameter values are required to account for these differences,
but most of the parameter values describing bone kinetics are generic, that is, the same foreach of these alkaline earth elements. The basis for applying generic values is discussed inearlier sections on calcium and strontium. Essentially, kinetic analysis of whole-bodyretention data for humans and more direct examination of alkaline earth kinetics in laboratory
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10046
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10048
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10051
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10057
10058
10059
10060
10061
10062
10063
10064
10065
10066
10067
10068
10069
10070
10071
10072
10073
10074
10075
10076
10077
10078
10079
10080
10081
10082
10083
10084
10085
10086
10087
10088
10089
10090
10091

animals do not reveal distinct differences between these elements with regard to thefollowing: early accumulation in bone as a fraction of activity reaching blood; initial division
between trabecular and cortical bone; early rate of loss from bone, interpreted for purposes ofthe present model as transfer from bone surfaces to plasma; the fraction subject tointermediate-term retention in bone, interpreted as transfer from bone surfaces toexchangeable bone volume; and the rate of removal from bone at times remote from uptake,interpreted as removal of non-exchangeable activity due to bone resorption. The following
generic parameter values are applied (see the earlier sections on calcium and strontium):
fractional deposition in bone = 0.25; fractional deposition in trabecular bone = 1.25 times thaton cortical bone; half-time on bone surface = 1 d, with 5/6 transferring to plasma and 1/6 toexchangeable bone volume; removal rate from non-exchangeable trabecular and cortical bonevolume = 18% and 3% y-1, respectively. The transfer rates for radium derived from thesegeneric parameter values are as follows: plasma to trabecular bone surface = (1.25/2.25) ×
0.25 × 70 d-1 = 9.72 d-1; plasma to cortical bone surface = (1/2.25) × 0.25 × 70 d-1 = 7.78 d-1;
trabecular or cortical bone surface to the corresponding exchangeable bone volume
compartment = (1/6) × ln(2)/1 d = 0.116 d-1, trabecular or cortical bone surface to plasma is(5/6) × ln(2)/1 d = 0.578 d-1; trabecular bone volume to plasma, 0.000493 d-1; and nonexchangeable cortical bone volume to plasma, 0.0000821 d-1.
(762) Observed differences in the behavior of alkaline earth elements in bone areaccounted for by differences in the rate of removal from the exchangeable bone volume
compartments and the fraction transferred from exchangeable to non-exchangeable bonevolume. It is assumed, in effect, that calcium, strontium, barium, and radium are all equally
likely to become temporarily incorporated in bone mineral after injection into blood but thatthe likelihood of reaching a non-exchangeable site in bone crystal decreases in the ordercalcium > strontium > barium > radium. Fractional transfers of calcium, strontium, barium,
and radium from exchangeable to non-exchangeable bone volume are set at 0.6, 0.5, 0.3, and0.2, respectively, and the balance is assumed to return to bone surfaces. The removal halftimes from exchangeable bone volume are set at 100 d, 80 d, 50 d, and 30 d, respectively.
These values are set to achieve reasonable consistency with whole-body retention curves forhumans injected with radioisotopes of the alkaline earth elements (e.g. Harrison et al., 1967;
Newton et al., 1977; Harrison, 1981; Newton et al., 1991). The assumed fractional transfers
to non-exchangeable bone volume are also reasonably consistent with results of in vitro
measurements. For example, under conditions approximating physiological, Neuman (1964)
found that calcium incorporated into forming hydroxyapatite crystals is 65% nonexchangeable, and Stark (1968) determined discrimination factors relative to calcium of 0.93
for strontium, 0.56 for barium, and 0.32 for radium in forming crystals. Such in vitro results
have varied to some extent with experimental conditions, length of aging of the crystals, andthe definition of discrimination (Neuman, 1964; Stark, 1968).
(763) For radium, the above estimates of the removal half-time from exchangeable bonevolume and the fractional transfers to non-exchangeable bone volume and bone surface yield
the following transfer rates: exchangeable to non-exchangeable bone volume (cortical ortrabecular), 0.2 × ln(2)/30 d = 0.0046 d-1; exchangeable bone volume to bone surface, 0.8 ×
ln(2)/30 d = 0.0185 d-1.
(764) Based on estimates from human studies (Looney et al., 1956; Schales, 1964;
Harrison et al., 1967; Maletskos et al.. 1969, Newton et al., 1991), it is estimated that 32% ofradium leaving plasma is deposited in excretion pathways and that the ratio of urinary tofaecal excretion is 1:36. The derived transfer rate from plasma to the urinary bladder contents

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10105
10106
10107
10108
10109
10110
10111
10112
10113
10114
10115

is 0.606 d-1 and from plasma to the contents of the right colon is 21.8 d-1.
(765) The transfer coefficients of the model for systemic radium in the worker are
summarized in Table 13-3.
13.2.3.3. Treatment of radioactive progeny
Dosimetrically significant progeny of radium(766) The radioactive progeny of radium isotopes addressed in this report are isotopes ofradon, polonium, lead, bismuth, thallium, actinium, thorium, radium, francium, or astatine.
Radon(767) A generic model is applied in this series of reports to radon, xenon, and krypton
produced in systemic compartments by decay of a parent radionuclide. These gases are
assigned the model for transfer of radon from bone to blood introduced in ICRP Publication
67 (1993) but are assigned element-specific rates of transfer from soft tissues to blood.
Specifically, radon, xenon, or krypton produced in non-exchangeable bone volume,
exchangeable bone volume, or bone surface transfers to blood at the rate 0.36 d-1, 1.5 d-1, or
100 d-1, respectively. Radon produced in a soft-tissue compartment transfers to blood with ahalf-time of 30 min, compared with a half-time of 20 min for xenon and 15 min for krypton.
Radon, xenon, or krypton produced in blood or entering blood after its production in asystemic compartment is removed from the body (exhaled) at the rate 1000 d-1, corresponding
to a half-time of 1 min.

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10116

Table 13-3. Transfer coefficients for radium

From
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Trabecular bone surface
Trabecular bone surface
Cortical bone surface
Cortical bone surface
ST0
ST1
ST2
Liver 1
Liver 1
Liver 2Kidneys 1
Kidneys 1
Kidneys 2
Exch trabecular bone volume
Exch trabecular bone volume
Exch cortical bone volume
Exch cortical bone volume
Nonexch cortical bone volume
Nonexch trabecular bone volume
10117
10118
10119
10120
10121
10122
10123
10124
10125
10126
10127
10128
10129
10130
10131
10132

To
Urinary bladder content
Right colon content
Trabecular bone surface
Cortical bone surface
ST0
ST1
ST2
Liver 1Kidneys 1
Blood
Exch trabecular bone volume
Blood
Exch cortical bone volume
Blood
Blood
Blood
Blood
Liver 2
Blood
Blood
Kidneys 2
Blood
Trabecular bone surface
Nonexch trabecular bone volume
Cortical bone surface
Nonexch cortical bone volume
Blood
Blood

Transfercoefficient
(d-1)
0.606
21.79
9.72
7.78
20.93
3.5
0.07
4.2
1.4
0.578
0.116
0.578
0.116
6.98
0.693
0.00038
0.691
0.002080.00192.073
0.006240.00190.01850.00460.01850.00460.0000821
0.000493

Polonium(768) The model for polonium produced in systemic compartments following intake of aradium isotope is a simplified version of the model applied in this report to polonium
absorbed to blood following its inhalation as a parent radionuclide. It is assumed thatpolonium leaves the central blood compartment of the model (Plasma) at the rate 100 d-1 anddistributes as follows: 5% to red blood cells (RBC), 3% to plasma proteins (Plasma P), 28%
to Liver, 28% to Kidneys, 1.2% to Bone surface, 3.3% to Trabecular marrow, 1.1% toCortical marrow, 1.6% to Spleen, 0.1% to Testes, 0.05% to Ovaries, 4% to a soft-tissuecompartment with a relatively long retention time (ST2), and the remaining 24.65% to a softtissue compartment with a relatively short retention time (ST1). Activity entering Liver isequally divided between compartments Liver 1 and Liver 2. Of the 28% of outflow from
Plasma depositing in Kidneys, 24% is assigned to the urinary path (Kidneys 1) and 4% is
assigned to other kidney tissue (Kidneys 2). Activity entering Bone surface is equally divided
between Cortical bone surface and Trabecular bone surface. Activity transfers to Plasma
from each of the compartments RBC, Plasma P, ST1, Liver 2, Trabecular marrow, Cortical255

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10133
10134
10135
10136
10137
10138
10139
10140
10141
10142
10143
10144
10145
10146
10147
10148
10149
10150
10151
10152
10153
10154
10155
10156
10157
10158
10159
10160
10161
10162
10163
10164
10165
10166
10167
10168
10169
10170
10171
10172
10173
10174
10175
10176
10177
10178
10179
10180

marrow, Spleen, and Kidneys 2 with a half-time of 7 d. Activity transfers from Liver 1 to
Small intestine content with a half-time of 5 d, from Kidneys 1 to Urinary bladder content
with a half-time of 4 d, from Trabecular and Cortical bone surface to Plasma with a half-timeof 30 d, from ST2 to Plasma with a half-time of 100 d, and from Testes and Ovaries to
Plasma with a half-time of 50 d. Polonium produced in a soft-tissue compartment of apreceding chain member that is not identifiable with a compartment in the polonium model isassumed to move to Plasma with a half-time of 7 d. Polonium produced in a compartment ofcortical or trabecular bone volume is assumed to transfer to Plasma at the reference rate ofturnover of that bone type.
Lead(769) The systemic model for lead as a progeny of radium is based on the characteristic
model for lead applied in this series of reports. The structure of the characteristic model ismodified by the addition of five compartments that are explicitly identified in models forsome elements appearing in radium chains: Trabecular marrow, Cortical marrow, Spleen,
Testes, and Ovaries. Each of these compartments is assumed to exchange lead with thecentral blood compartment of the lead model (Plasma). Transfer coefficients are selected forreasonable consistency with the biokinetic database underlying the characteristic model forlead and with the retention curve for total soft tissues based on that original model. The
specific changes to the characteristic model for lead are as follows: (1) the transfer
coefficients from Plasma to compartments added to the characteristic model for lead are
0.015 d-1 for Trabecular marrow, 0.005 d-1 for Cortical marrow, 0.002 d-1 for Spleen, 0.00045
d-1 for Testes, and 0.00015 d-1 for Ovaries; (2) the transfer coefficient from Plasma to ST1 isreduced from 0.70 d-1 to 0.681 d-1, and the coefficient from Plasma to ST2 is reduced from
0.14 d-1 to 0.136 d-1; and (3) the assigned transfer coefficient from each of the added
compartments back to Plasma is 0.002 d-1. Lead produced in a blood compartment of apreceding chain member that is not identifiable with a blood compartment of the lead modelis assigned the transfer rate 1000 d-1 to Plasma.
Bismuth(770) The systemic model for bismuth as a progeny of radium is based on the characteristic
model for bismuth applied in this series of reports. The structure of the characteristic model
is modified by the addition of five compartments that are explicitly identified in models forsome elements appearing in radium chains: Trabecular marrow, Cortical marrow, Spleen,
Testes, and Ovaries. Each of these compartments is assumed to exchange lead with thecentral blood compartment of the bismuth model. Transfer coefficients for these added
compartments are selected for reasonable consistency with the biokinetic database underlying
the characteristic model for bismuth and with the retention curve for total soft tissues basedon that original model. The specific changes to the characteristic model for bismuth are as
follows: (1) the transfer coefficients from plasma to the added compartments are 0.3 d-1 forTrabecular marrow, 0.1 d-1 for Cortical marrow, 0.02 d-1 for Spleen, 0.003 d-1 for Testes, and
0.001 d-1 for Ovaries; (2) the transfer coefficient from plasma to the Other soft-tissuecompartment ST1 is reduced from 4.2 d-1 to 3.876 d-1, and the coefficient from plasma to the
Other soft tissue compartment ST2 is reduced from 1.3 d-1 to 1.2 d-1; and (3) the assigned
transfer coefficient from each of the added compartments back to plasma is 0.007 d-1 (halftime of 100 d). Bismuth produced in a blood compartment that is not identifiable with acompartment of the bismuth model is assumed to transfer to the plasma compartment of thebismuth model at the rate 1000 d-1. Bismuth produced in a trabecular or cortical bone volume256

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10181
10182
10183
10184
10185
10186
10187
10188
10189
10190
10191
10192
10193
10194
10195
10196
10197
10198
10199
10200
10201
10202
10203
10204
10205
10206
10207
10208
10209
10210
10211
10212
10213
10214
10215
10216
10217
10218
10219
10220
10221
10222
10223
10224
10225
10226
10227
10228

compartment is assumed to transfer to plasma at the reference turnover rate for that bone type.
Thallium(771) The section on lead contains a summary of biokinetic information on systemic
thallium and a biokinetic model for thallium produced in systemic compartments following
intake of a radioisotope of lead. The following modified version of that model is applied tothallium produced in systemic compartments following intake of a radioisotope of radium.
Thallium leaves the central blood compartment (Plasma) at the rate 200 d-1 (corresponding toa half-time of 5 min) and is distributed as follows: 2.5% to RBC, 0.75% to Urinary bladdercontent, 1.75% to Right colon content, 5% to Kidneys, 5% to Liver, 1.5% to Trabecularmarrow, 0.5% to Cortical marrow, 0.2% to Spleen, 0.045% to Testes, 0.015% to Ovaries,
7.5% to Trabecular bone surface, 7.5% to Cortical bone surface, and 67.74% to ST0(remaining soft tissues). Thallium returns from RBC to Plasma at the rate 3.7 d-1 and fromtissue compartments to Plasma at the rate 2.5 d-1. Thallium produced by radioactive decay ina blood compartment that is not identifiable with a compartment of the thallium model isassumed to transfer to Plasma at the rate 1000 d-1. Thallium produced in a soft-tissuecompartment that is not identifiable with a compartment of the thallium model is assumed totransfer to Plasma at the rate 2.5 d-1. Thallium produced in a compartment of cortical ortrabecular bone volume is assumed to transfer to Plasma at the reference turnover rate of thatbone type.
Actinium(772) Studies on laboratory animals indicate that the systemic behavior of actinium isbroadly similar to that of americium (USEPA, 1999; NCRP, 2009). The model for systemic
americium adopted in ICRP Publication 67 (1993) is applied here to actinium as a progeny ofradium. Actinium produced in a compartment of a preceding chain member that is not
identifiable with a compartment in the actinium model is assumed to transfer to the central
blood compartment of the actinium model at the following rate: 0.0019 d-1 (half-time of 1 y)if produced in the liver; and at the rate of bone turnover if produced in the exchangeable bonevolume compartment of trabecular or cortical bone.
Thorium(773) The systemic model applied to thorium as a parent radionuclide in this series ofreports is also applied to thorium produced in systemic compartments following intake of aradium isotope. Thorium produced in an exchangeable bone volume compartment in themodel of a preceding chain member is assumed to transfer to the central blood compartmentof the thorium model at the rate of bone turnover.
Radium(774) The model for radium as a parent radionuclide is also applied to radium produced byserial decay of members of a radium chain. Radium produced in a compartment of apreceding chain member that is not identifiable with a compartment in the radium model isassumed to transfer to the central blood compartment of the radium model at the following
rates: 1000 d-1 if produced in a blood compartment and 0.693 d-1 (half-time of 1 d) if
produced in a soft-tissue compartment. The value 0.693 d-1 is the transfer coefficient from theintermediate-term soft tissue compartment ST1 to blood in the characteristic model forradium.

257

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10229
10230
10231
10232
10233
10234
10235
10236
10237
10238
10239
10240
10241
10242

Francium and astatine(775) Radioisotopes of francium and astatine appearing in radium chains considered in thisreport have half-lives varying from <1 s to 22 min. These short-lived radionuclides are
assumed to decay at their sites of production.
13.3.

Individual Monitoring

226

Ra(776) 226Ra intakes are generally determined though analysis of its excretion in urine.
Several measurement techniques may be used: alpha spectrometry, beta counting in a
proportional counter or liquid scintillation counting, after chemical separation and emanationof 222Rn into a scintillation cell for measurement of photon emissions from its short-lived
progeny.
IsotopeMonitoring
Technique

226

Urine Bioassay

Ra

226

Ra
Ra

Urine Bioassay
Urine Bioassay

226

Ra

Urine Bioassay

226

Ra

Faeces Bioassay

226

10243
10244
10245
10246
10247
10248
10249
10250

10251
10252
10253
10254
10255

MethodMeasurementof Typical
DetectionLimit
α spectrometry
10 m Bq/L
Emanation
Proportionalcounter
Liquid scintillation
counting
Proportional
Counter

Achievabledetection limit

5 mBq/L
4 mBq/L
3mBq/L
16mBq/24h

228Ra(777) 228Ra intakes may be determined though analysis of its excretion in urine, using beta
counting in a proportional counter or liquid scintillation counting, after chemical separation
Bioassay monitoring using faeces samples is also possible.
(778) Ra-228 cannot be detected directly by in vivo measurement. The lung content of Ra228 can be inferred from a measurement of its immediate decay product, Ac-228.
IsotopeMonitoring
Technique

228

Ra

Urine Bioassay

228

Ra

Urine Bioassay

228

Ra

Faeces Bioassay

228

Ra

LungCounting

MethodMeasurementof Typical
Detection
Limit
Beta Proportional 1 Bq/L
counter
Liquid scintillation 50mBq/L
counting
Beta Proportional 0.1Bq/24h
counter
γ-ray spectrometry 40 Bq
of 228Ac

Achievabledetection limit
0.01 Bq/L

15 Bq

References
Atherton, D.R., Stover, B.J., Mays, C.W., 1965. Soft tissue retention of Ra-226 in the beagle. Health258

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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10257
10258
10259
10260
10261
10262
10263
10264
10265
10266
10267
10268
10269
10270
10271
10272
10273
10274
10275
10276
10277
10278
10279
10280
10281
10282
10283
10284
10285
10286
10287
10288
10289
10290
10291
10292
10293
10294
10295
10296
10297
10298
10299
10300
10301
10302
10303
10304
10305
10306
10307

Phys. 11, 101-108.
Ballou, J.E., Gies, R.A., Case, A.C., Huggard, D.L., Buschbom, R.L., Ryan, J.L., 1986. Depositionand early disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat. Health Phys.
51, 755–771.
Cuddihy, R.G., Griffith, W.C., 1972. A biological model describing tissue distribution and wholebody retention of barium and lanthanum in beagle dogs after inhalation and gavage. HealthPhys., 23, 621-633.
Della Rosa, R.J., Goldman, M., Wolf, H.G., 1967. Uptake and retention of orally administered Ra226 and Ba-133: A preliminary report, University of California at Davis, Report 472-114,
pp. 40-41.
Glad, B. W.; Mays, C. W.; Fisher, W. 1960. Strontium studies in beagles. Radiat. Res. 12, 672-681.
Hardy, E., Rivera, J., Fisenne, I., Pond, W., Hogue, D., 1969. Comparative utilization of dietaryradium-226 and other alkaline earths by pigs and sheep. In: Sikov, M.R., Mahlum, D.D.
(Eds), Radiation biology of the fetal and juvenile mammal. Proc. of the ninth annual
Hanford biology symposium at Richland, Washington, May 5-8, 1969; U. S. AEC, Divisionof Technical Information, 183-190.
Harrison, G.E., 1981. Whole body retention of the alkaline earths in adult man. Health Phys., 40, 9599.
Harrison, G.E., Carr, T.E.F., Sutton, A., 1967. Distribution of radioactive calcium, strontium, bariumand radium following intravenous injection into a healthy man. Int. J. Radiat. Biol., 13, 235247.
Hursh, J.B., Lovaas, A., 1963. Radium-226 in bone and soft tissues of man. Nature 198, 265-268.
ICRP, 1973. Alkaline Earth Metabolism in Adult Man, Publication 20, Pergamon Press, Oxford.
ICRP, 1979. Limits on Intakes of Radionuclides for Workers. ICRP Publication 30, Part 1. Ann.
ICRP 2. (3/4).
ICRP, 1993. Age-dependent Doses to Members of the Public from Intake of Radionuclides: Part 2,
Ingestion dose coefficients . ICRP Publication 67. Ann. ICRP 23. (3/4).
ICRP, 1995. Age-dependent Doses to Members of the Public from Intake of Radionuclides: Part 4
Inhalation dose coefficients. ICRP Publication 71. Ann. ICRP 25(3-4), 393-405.
Kalkwarf, D.R., Jackson, P.O., Hardin, J.M., 1984. Lung-clearance classification of radionuclides incoal fly ash. Health Phys., 47, 37–45.
Keane, A.T., Schlenker, R.A., 1987. Long-term loss of radium in 63 subjects exposed at ages 6 to 46.
In: Age-related factors in radionuclide metabolism and dosimetry, ed. G. B. Gerber, H.
Metivier, H. Smith. Proceedings of a workshop in Angers, November 26-28, 1986;
Dordrecht: Martinus Nijhoff Publishers, 127-135.
Leggett, R.W., 1992. A generic age-specific biokinetic model for calcium-like elements, Radiation
Protection Dosimetry 41, 183-198.
Lloyd, R.D., Bruenger, F.W., Jones, C.W., Taylor, G.N., Mays, C.W., 1983a. Retention in mature
beagles injected at 5 years of age. Radiat. Res., 94, 210-216.
Lloyd, R.D., Bruenger, F.W., Mays, C.W., Jones, C.W., 1983b. Skeletal radon-to-radium ratios inneonatal, juvenile and mature beagles and in adult St. Bernards. Health Phys. 44:61-63.
Lloyd, R.D., Jones, C.W., Bruenger, F.W., Atherton, D.R., Mays, C.W., 1983c. Radium retention anddosimetry in juvenile beagles. Radiat. Res., 94, 295-304.
Lloyd, R.D., Taylor, G.N., Jones, C.W., Mays, C.W., 1983d. Radium retention and dosimetry in the
St. Bernard. Radiat. Res., 95, 150-157.
Lloyd, R.D., Mays, C.W., Atherton, D.R., 1976a. Distribution of injected Ra-226 and Sr-90 in the
beagle skeleton. Health Phys., 30, 183-189.
Lloyd, R.D., Mays, C.W., Atherton, D.R., Taylor, G.N., Van Dilla, M.A., 1976b. Retention andskeletal dosimetry of injected Ra-226, Ra-228, and Sr-90 in beagles. Radiat. Res., 66, 274287.
Lloyd, R.D., Mays, C.W., Taylor, G.N., Atherton, D.R., Bruenger, F.W., Jones, C.W., 1982. Radium224 retention, distribution, and dosimetry in beagles. Radiat. Res., 92, 280-295.

259

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10308
10309
10310
10311
10312
10313
10314
10315
10316
10317
10318
10319
10320
10321
10322
10323
10324
10325
10326
10327
10328
10329
10330
10331
10332
10333
10334
10335
10336
10337
10338
10339
10340
10341
10342
10343
10344
10345
10346
10347
10348
10349
10350
10351
10352
10353
10354
10355
10356
10357
10358
10359

Looney, W.B., Hursh, J.B., Archer, V.E., Steadman, L.T., Colodzin, M., 1956. A summary of radium
and thorium excretion in humans. In: Proceedings of the international conference on thepeaceful uses of atomic energy. Vol. 11. Biological effects of radiation. United Nations, pp.
55-64.
Looney, W.B., Archer, V.E., 1956. Radium inhalation accident - radium excretion study. Am. J.
Roentgenol. Rad. Ther. Nucl. Med., 75, 548-558.
Maletskos, C.J., Keane, A.T., Telles, N.C., Evans, R.D., 1969. Retention and absorption of Ra-224
and Th-234 and some dosimetric considerations of Ra-224 in human beings. In: Delayed
effects of bone-seeking radionuclides, ed. by C.W. Mays, W.S.S. Jee, R.D. Lloyd, B.J.
Stover, J.H. Dougherty, G.N. Taylor, Salt Lake City, UT, University of Utah Press, 29-49.
Maletskos, C.J., Keane, A.T., Trelles, N.C., Evans, R.D., 1966. The metabolism of intravenously
administered radium and thorium in human beings and the relative absorption from thehuman gastrointestinal tract of radium and thorium in simulated radium dial paints. Annual
Report MIT-952-3, Radioactivity Center, Inst Technology, Cambridge, MA. Pp.202-317.
Marinelli, L.D., Norris, W.P., Gustafson, P.F., Speckman, T.W., 1953. Transport of radium sulfate
from the lung and its elimination from the human body following single accidental
exposures. Radiology 61, 903–915.
Mays, C.W., Christensen, W.R., Lloyd, R.D., Atherton, D.R., Parmley, W.W., Pitchford, G.S., 1962.
Radium studies in a man soon after injection. In: Research in radiobiology, COO-226, Univ.
of Utah, 71-77.
Mays, C.W., Lloyd, R.D., Christensen, W.R., Atherton, D.R., Pitchford, G.S., 1963. Radium
metabolism in a man. Radiat. Res., 19, 210.
Miller, C.E., Finkel, A.J., 1965. A re-examination of retention patterns in patients who received
radium by multiple injections 33 years earlier. In: Health division gamma-ray spectroscopy
group annual report, July 1964 through June 1965, Argonne National Laboratory, ANL7217; 5-90.
Moody, J.C., Stradling, G.N., 1992. Biokinetics of thorium and daughter radionuclides after
deposition in the rat lung. J. Aerosol Sci., 23, Suppl. 1, S523–S526.
NCRP 2009. Management of persons contaminated with radionuclides. NCRP Report No. 161.
National Council on Radiation Protection and Measurements: Bethesda, Maryland.
Neuman, W.F., 1964. Blood-bone exchange. In: Bone biodynamics, ed. by H.M. Frost. Boston: Little,
Brown, and Co, 393-408.
Newton, D., Harrison, G.E., Kang, C., Warner, A.J., 1991. Metabolism of injected barium in six
healthy men. Health Phys., 61, 191-201.
Newton, D., Rundo, J., Harrison, G.E., 1977. The retention of alkaline earth elements in man, withspecial reference to barium. Health Phys., 33, 45-53.
Norris, W.P., Speckman, T.W., Gustafson, P.F., 1955. Studies on the metabolism of radium in man.
Am. J. Roentgenol., Radium Ther. Nucl. Med., 73, 785-802.
Parks, N.J., Keane, A.T., 1983. Consideration of age-dependent radium retention in people on thebasis of the beagle model. Health Phys., 44, 103-112.
Parks, N.J., Pool, R.R., Williams, J.R., Wolf, H.G., 1978. Age and dosage-level dependence ofradium retention in beagles. Radiat. Res., 75, 617-632.
Qiyue, H., Zhonghon, Z., Shijun, L., 1988. Radium-226: Concentration and distribution in humanbone. Chin. J. Radiol. Med. Prot. 8:224-225 (abstract).
Rajewsky, B., Belloch-Zimmermann, V., Loehr, E., Stahlhofen, W., 1965. Ra-226 in humanembryonic tissue, relationship of activity to the stage of pregnancy, measurement of natural
Ra-226 occurrence in the human placenta. Health Phys., 11, 161-169.
Schales, F., 1964. The excretion of thorium X and its daughter products after intravenous injection inman. In: Assessment of radioactivity in man, Vol. II, Vienna, IAEA, 267-276.
Schlenker, R.A., Keane, A.T., Holtzman, R.B., 1982. The retention of Ra-226 in human soft tissue
and bone; implications for the ICRP 20 alkaline earth model. Health Phys., 42, 671-693
1982.

260

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10360
10361
10362
10363
10364
10365
10366
10367
10368
10369
10370
10371
10372
10373
10374
10375
10376
10377
10378
10379
10380
10381
10382
10383

Schlundt, H., Nerancy, J.T., Morris, J.P., 1933. The detection and estimation of radium in living
persons. IV. The retention of soluble radium salts administered intravenously. Am. J.
Roentgenol., Radium Ther., 30, 515-522.
Seil, H, Viol, C, Gorden, M., 1915. The elimination of soluble radium salts taken intravenously andper os. Radium., 5, 40-44.
Stark, G., 1968. Studies on synthetic hydroxyapatite crystals with regard to metabolism of calcium,
strontium, barium and radium in bone. I. The discrimination against calcium. Biophysik, 5,42-54.
Taylor, D.M., Bligh, P.H., Duggan, M.H., 1962. The absorption of calcium, strontium, barium, andradium from the gastrointestinal tract of the rat. Biochem. J., 83, 25-29.
Toohey, R.E., Sha, J.Y., Urnezis, P.W., Hwang, E.Y., 1984. An unusual case of radium exposure.
Argonne National Laboratory Environmental Research Division Annual Report July 1982 –June 1983, ANL–83–100 Part II, 15–20.
USEPA 1999. Cancer risk coefficients for environmental exposure to radionuclides. Federal
Guidance Report No. 13, EPA 402-R-99-001. Prepared by Eckerman, K. F.; Leggett, R. W.;
Nelson, C. B.; Puskin, J. S.; Richardson, A. C. B. Office of Radiation and Indoor Air. US
Environmental Protection Agency: Washington, D.C.
Van Dilla, M.A., Stover, B.J., Floyd, R.L., Atherton, D.R., Taysum, D.H., 1958. Radium (Ra-226)
and radon (Em-222) metabolism in dogs. Radiat. Res., 8, 417-437.
Wood, S.K., Farnham, J.E., Marshall, J.H., 1970. Ca-45, Ba-133, and Ra-226 in 6-to 10-year-old
beagle dogs: A 100-day study. In: Radiological Physics Division annual report, Center for
Human Radiobiology, July 1969 through June 1970; Argonne, IL: Argonne National
Laboratory; ANL-7760, Part II, Biology and Medicine, 110-132.

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10384
10385
10386
10387
10388
10389
10390
10391
10392
10393
10394
10395
10396
10397

14.
14.1.

Chemical Forms in the Workplace(779) Thorium is an actinide element which occurs mainly in oxidation state IV. It isnaturally abundant in the earth and the main ores are thorite, thorianite, and monazite, thelatter occurring mainly as mineral sand. Thorium may be encountered in industry in a varietyof chemical and physical forms, such as oxides (ThO2), hydroxides, nitrates, fluorides andsulphates.
(780) Thorium-232 can be used as fuel in a nuclear reactor to absorb slow neutrons and to
produce 233U, which is fissile.
Table 14-1. Isotopes of thorium addressed in this report
IsotopeTh-226
Th-227
Th-228a
Th-229a
Th-230a
Th-231
Th-232a
Th-233
Th-234aTh-236

10398
10399
10400
10401
10402
10403
10404
10405
10406
10407
10408
10409
10410
10411
10412
10413
10414
10415
10416
10417
10418
10419
10420

Thorium (Z = 90)

a

14.2.

Physical half-life
30.57 m18.68 d1.912 y7.34E+3 y
7.538E+4 y
25.52 h1.405E+10 y22.3 m24.10 d37.5 mDecay mode
A
A
A
A
A
BA
BBB-

Data for these radionuclides are given in the printed copy of this report. Data for otherradionuclides are given on accompanying electronic disk.

Routes of Intake

14.2.1. Inhalation
Absorption Types and parameter values(781) Information is available on the biokinetic behaviour of thorium after deposition ofvarious chemical forms in the respiratory tract after accidental human exposure, and fromexperimental studies with animals, mainly rats.
(782) Absorption parameter values and Types, and associated fA values for particulate
forms of thorium are given in Table 14-2. In referring to default types it should be noted thatthe biokinetic behaviour of thorium is exceptional in that, following deposition of watersoluble forms in the lungs, a minor fraction of the lung deposit is absorbed very rapidly, after
which absorption is minimal. This indicates that there are no commonly encountered Type F
forms of thorium.
Thorium chloride (ThCl4)(783) Boecker et al. (1963) conducted a series of experiments to determine the effect of themass of thorium deposited in the lungs on its disposition, by following the biokinetics of234
Th (half-life 24 days) for up to 90 days after inhalation of the chloride by rats. Theyobserved that soon after exposure a fraction of the thorium deposited in the lungs was

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absorbed into the body, but after this the thorium organ contents remained approximately
constant: the lung content decreased with time, with excretion of thorium predominantly infaeces. Similar behaviour has been observed following deposition of other water-soluble
thorium compounds in the lungs: see below. It suggests that the fraction of thorium that is notabsorbed rapidly is retained in the lungs in particulate form, rather than bound to respiratory
tract tissues. They also found that the fraction of the thorium initial lung deposit (ILD) that
was absorbed, and the fractions excreted in the urine and faeces, did not appear to be affectedby variation in the mass of the ILD by a factor of 105. This was in contrast to mass-dependent
biokinetics observed by Thomas et al. (1963) following injection by different routes,
including intratracheal instillation. It was considered that this might be due to the relatively
high local concentrations that occurred in the injection studies, compared to the more diffuse(in both space and time) distribution following inhalation. At the first measurement of
distribution, made <1 hour after exposure, the “Remainder” tissue (taken by the authors to
represent activity absorbed from the lungs), contained about 10% ILD, and showed little
further change. This indicated that the absorption rate corresponds to a time constant of lessthan an hour, i.e. that sr was more than 20 d–1. However, it was not very much greater,
because it appeared that clearance from the upper respiratory tract (URT) was mainly to thealimentary tract. At this time there were similar amounts of thorium in the URT and in thealimentary tract plus contents, indicating that the particle transport rate from the URT was
about 20 d–1: this was assumed in all the assessments carried out here (i.e. by the Task Group)for thorium inhaled by rats. The lung content decreased from about 85% ILD at 6 d to 28%
ILD at 84 d. Absorption parameter values of fr = 0.06, sr = 90 d–1 and ss = 0.002 d–1 wereassessed here. Retention in lung and carcass were represented well, without the need to
introduce the bound state.
(784) Boecker (1963) followed the biokinetics of 234Th for 32 days after inhalation of thechloride by rats. At the first measurement of distribution, made <1 hour after exposure, the“Remainder” tissue contained ~7% ILD, which increased to ~15% at 2 days onwards.
Absorption parameter values of fr = 0.13, sr = 20 d–1 and ss = 0.004 d–1 were assessed here.
Boecker also found that thorium in rats exposed up to five times behaved similarly to thorium
in rats exposed only once.
Water-soluble forms of thorium and Type F thorium(785) Based on the results of the experiments outlined above, and those with thorium
citrate and nitrate below, specific dissolution parameter values of fr = 0.1, sr = 50 d–1 and ss =0.005 d–1 (consistent with assignment to default Type M) are used here for water-soluble
forms of thorium, including chloride. It should be noted that with an initial uptake as high as~10% ILD, it is difficult to estimate the low value of ss. This consideration also applies to thefollowing compounds that are assigned to Type M. Since the estimated values of ss are close
to the Type M default value of 0.005, it was used. The values of sr, with those estimated forchloride (below), are also used here to assign the specific value of sr for Type F thorium.
Default Type F thorium (with dissolution parameter values: fr = 0.1, sr = 50 d–1) isnevertheless retained as an option.
Thorium citrate(786) Thomas et al. (1963) measured the tissue distribution of 234Th at times from 7 to 19
days after intratracheal instillation into rats as the citrate, as a preliminary to inhalation
experiments (see below for citrate, and above for chloride). There was no obvious changewith time and mean values were reported. When administered at tracer level, ~3% ILD
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remained in the lungs and ~50% was absorbed (deposited in systemic organs). Whenadministered with carrier, ~10% ILD remained in the lungs, and ~15% was absorbed,
indicating Type F and Type M behaviour respectively.
(787) Boecker (1963) followed the biokinetics of 234Th for 32 days after inhalation of thecitrate by rats. The first measurement of distribution was made soon (<1 hour) after
exposure. The “Remainder” tissue, taken by the author to represent activity absorbed fromthe lungs, already contained about 40% ILD, and showed little further change. This was morethan found for the chloride in a similar experiment (~10% ILD, see above) but suggests thatas for the chloride sr was more than 20 d–1, but not much greater. About 60% ILD remained in
the lungs at 7 days, much more than after intratracheal instillation (see above) and it wassuggested that the difference was an artefact of the instillation procedure. Absorption
parameter values of fr = 0.14, sr = 70 d–1 and ss = 0.01 d–1 were assessed here, giving
assignment to Type M.
(788) Based on the results of the experiments outlined above, and those with thorium
chloride (above) and nitrate (below), specific absorption parameter values of fr = 0.1, sr = 50
d–1 and ss = 0.005 d–1 (consistent with assignment to default Type M) are used here for watersoluble forms of thorium, including citrate. The values of sr, with those estimated for chloride(above), are also used here to assign the specific value for Type F thorium.
Thorium nitrate (Th(NO3)4)(789) Ballou et al. (1986) measured the tissue distributions of 232U and its decay products
at 24 hours after their intratracheal instillation into rats as nitrates. (For further information
see the uranium inhalation section, and the section below on decay products of thorium
formed in the respiratory tract.) For 228Th, lung retention was 52% ILD, much higher than forthe other radionuclides, with deposition in the skeleton at 12% ILD, broadly similar to the
behaviour observed after instillation of thorium sulphate (see below).
(790) Gray et al. (1991) measured the tissue distribution of 230+232Th at times between 7
and 252 days after administration to rats by inhalation or intratracheal instillation of thorium
nitrate with an ILD of about 5 µg thorium. Following inhalation, lung retention decreased
from 73% ILD to 12.6% ILD between 7 and 252 days. It was estimated that about 10% was
absorbed by 7 days, with little subsequent change. Thus the overall behaviour was similar tothat observed for inhaled chloride and citrate (see above). With the first measurement at 7days, there is no information on which sr can be estimated. Stradling et al. (2004) derived
two sets of parameter values from the data: assuming a “low” value for sr of 3 d–1, gave fr =0.07 and ss = 0.00035 d–1; assuming a “high” value for sr of 100 d–1, gave fr = 0.04 and ss =0.0005 d–1. Values of sr in the range 20–90 d–1 were obtained here from the results ofinhalation experiments with chloride and citrate (see above). Taking a central value of 50 d–1,
a good fit to the data was obtained here with fr = 0.04 and ss = 0.0008 d–1, giving assignment
to Type M. Very similar values were obtained for the data following instillation (fr = 0.05 andss = 0.0008 d–1).
(791) Gray et al. (1991) also followed the biokinetics of thorium after intratracheal
instillation into rats of thorium nitrate with ILDs of about 2 pg or 3 ng thorium, with the firstmeasurement at 1 or 7 days and the last at 28 or 84 days. Assuming sr = 50 d–1, and ss =0.0008 d–1 (as in the longer-term studies) values of fr of about 0.3 were obtained here for both
(giving assignment to Type M). Thus a larger fraction was absorbed rapidly when these lower
masses were instilled, as observed by Thomas et al. (1963) for thorium citrate.
(792) Moody et al. (1994a; Moody and Stradling, 1992) measured the tissue distributionsof 228Th, 212Pb, 212Bi and 208Tl, at times from 6 hours to 7 days after intratracheal instillation
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into rats of a nitrate solution of 228Th in equilibrium with its decay products (ILD 17 ng Th).
(For further information see the section below on decay products of thorium formed in the
respiratory tract.) For thorium, about 20% ILD was absorbed by 6 hours, with little
subsequent change, indicating that sr was more than 4 d–1. They also measured the tissue
distribution of 228Th at times from 1 to 84 days after instillation of Th nitrate (ILD 32 ng).
Assuming sr = 50 d–1, and ss = 0.0008 d–1 (as above) values of fr of 0.2 and 0.14 respectively
were obtained here.
(793) Stradling et al. (2005a) measured the tissue distribution of 228Th at times from 1 to84 days after intratracheal instillation into rats of a nitrate solution of 228Th. Absorption was
somewhat greater for an ILD of 1.6 pg thorium than for an ILD of 0.17 µg thorium. Assuming
sr = 50 d–1, and ss = 0.0008 d–1 (as above) values of fr of 0.35 and 0.25 were obtained here.
The behaviour of thorium was not significantly affected by the presence of uranium when
they were administered together (for further information, see section on decay products ofuranium formed in the respiratory tract).
(794) Thus similar overall behaviour was reported in these experiments, with absorption toblood largely complete by the time of the first measurement. The studies with citrate andchloride outlined above suggest that following inhalation there is little effect of mass on the
biokinetics of thorium, but following instillation the rapidly absorbed fraction decreases withmass instilled. Similarly, for thorium nitrate administered by instillation, the fraction of ILD
absorbed rapidly tends to decrease with increasing ILD. Values of fr estimated here varied
from 0.05 to 0.35, (giving assignment to Type M) with the lowest value at the highest ILD. A
value of fr = 0.04 was obtained from the results of the only inhalation experiment withthorium nitrate (Gray et al., 1991). Based on the results of the experiments outlined above,and those with thorium chloride and citrate, specific absorption parameter values of fr = 0.1, sr= 50 d–1 and ss = 0.005 d–1 (consistent with assignment to default Type M) are used here forwater-soluble forms of thorium, including nitrate.
Thorium sulphate (Th(SO4)2)(795) Scott et al. (1952) measured the tissue distribution of 234Th at 4 days after
intratracheal instillation into rats of thorium sulphate solution (with carrier). About 35% ILD
remained in the lungs and 4% was deposited in systemic organs indicating somewhat lessabsorption than for instillation of thorium citrate (see above), but also indicating Type M
behaviour. Since the thorium sulphate was administered in solution the specific parametervalues adopted here for water-soluble forms of thorium (fr = 0.05, sr = 50 d–1, and ss = 0.001d–1) are also applied to thorium sulphate.
Thorium fluoride (ThF4)(796) Stradling et al. (2005b; Moody et al., 1994b) measured the tissue distributions of
228
Th, 212Pb, 212Bi and 208Tl, at times from 1 to 168 days after intratracheal instillation into
rats of a suspension of 228Th or 228+232Th fluoride (ILD 60 pg or 6.5 µg thorium) inequilibrium with the decay products of 228Th. (For further information see the section below
on decay products of thorium formed in the respiratory tract.) As for the water-soluble forms(see above) absorption of thorium to blood was largely complete by the time of the firstmeasurement. However, the authors noted that although the tissue distribution of systemic
thorium was independent of mass or chemical form administered, the fraction excreted
rapidly in urine was much higher than observed for the nitrate, and suggested that this mightreflect the transfer of ultrafine particles through the kidneys. Lung retention at 168 days was
greater with the higher mass than with the lower mass administered (25% vs 8% ILD),
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presumably because particle transport was impaired. Estimated absorption in the first day
was greater for an ILD of 60 pg (12% ILD) than for an ILD of 6.5 µg thorium (6% ILD).
Assuming sr = 50 d–1, (as above, since most absorption took place within 1 d) values of fr of
0.10 and 0.06, respectively and values of ss of 0.003 d–1 and 0.001 d–1 respectively wereobtained here, giving assignment to Type M. The parameter values assessed are similar to
those adopted here for water-soluble forms of thorium (fr = 0.1, sr = 50 d–1 and ss = 0.005 d–1)
and therefore these specific absorption parameter values are also used here for thorium
fluoride.
Thorium hydroxide (Th(OH)4)(797) Albert (1966), in a review of lung retention of thorium, referred to a study in which
about 2% ILD of the thorium was absorbed from the lungs in 2 months after intratracheal
instillation of Th(OH)4 into rats (Thomas R. G., The Metabolism of Thorium-230 (Ionium)
Administered by Intratracheal Injection to the Rat. USAEC Report UR-40, University ofRochester, January 1957).
(798) Stradling et al. (2005b; Moody et al., 1994b) measured the tissue distributions of
228
Th, 212Pb, 212Bi and 208Tl at times from 1 to 168 days after intratracheal instillation into ratsof a suspension of 228Th or 228+232Th hydroxide (ILD 50 pg or 6.5 µg thorium) in equilibriumwith the decay products of 228Th. (For further information see the section below on decay
products of thorium formed in the respiratory tract.) Results were similar to those obtained
for the fluoride. Absorption to blood was largely complete by the time of the firstmeasurement. However, the authors noted that although the tissue distribution of systemic
thorium was independent of mass or chemical form administered, the fraction excreted
rapidly in urine was much higher than observed for the nitrate, and suggested that this mightreflect the transfer of ultrafine particles through the kidneys. Lung retention at 168 days was
greater with the higher mass than with the lower mass administered (17% vs 8% ILD),
presumably because particle transport was impaired. Estimated absorption in the first day was
somewhat greater for an ILD of 50 pg (8% ILD) than for an ILD of 6.5 µg thorium (6% ILD).
Assuming sr = 50 d–1, (as above, since most absorption took place within 1 d) values of fr of
0.07 and 0.06, respectively and values of ss of 0.002 d–1 and 0.001 d–1 respectively wereobtained here, giving assignment to Type M. The parameter values assessed are similar to
those adopted here for water-soluble forms of thorium (fr = 0.1, sr = 50 d–1 and ss = 0.005 d–1)
and therefore these specific absorption parameter values are also used here for thoriumhydroxide.
Thorium dioxide (ThO2)(799) Hodge and Thomas (1959) reported that high concentrations of thorium were foundin the lungs and lymph nodes of dogs sacrificed 7 years after 2-year inhalation exposure to
ThO2. Few details are given but the authors inferred that negligible amounts of thorium had
cleared from the lungs in 7 years, indicating Type S behaviour.
(800) Newton et al. (1981) followed the retention of 228Th for 7 years in a man who
became internally contaminated, presumably through its inhalation in oxide form. The firstmeasurements were made about 500 days after the presumed time of intake. The authors
assessed that by this time only a small fraction of the 228Th in the body was in the lungs,
suggesting Type M rather than Type S behaviour.
(801) Ballou and Hursh (1972) followed retention of 228Th in the lungs of dogs for 150
days after inhalation of ThO2, by in vivo measurements of exhaled thoron (220Rn) and 208Tl
gamma emissions over the thorax, and post mortem measurements of 228Th in the lungs. At
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14 days, about 1% ILD was in the body outside the lungs, indicating that fr was ~0.01. The
authors estimated lung retention half-times of 350–500 days, suggesting Type S behaviour.
(See also the section below on decay products of thorium formed in the respiratory tract.)(802) Lamont et al. (2001) measured the dissolution rates in simulated lung fluid of freshly
prepared and aged samples of ThO2 for 100 days. The fractions dissolved over 100 days were
~2x10–6 and 1x10–5 respectively. The higher value for the aged oxide was attributed toradiolytic damage and consequent increase in surface area. Most of the dissolution occurredin the first day or so, giving values of fr ~2x10–6 and 1x10–5, and values of ss less than ~10–7
d–1 and 10–8 d–1 respectively.
(803) Hodgson et al. (2000, 2003) measured the tissue distributions of 228Th, 212Pb, 212Bi
and 208Tl, at times from 1 to 168 days after intratracheal instillation into rats of suspensions of
232
Th dioxide enriched with 228Th in equilibrium with its decay products, with two different
particle sizes (geometric diameters about 0.4 and 2 µm). About 1% ILD was measured in the
carcass at the first measurement (6 hours), with no further measurable increase, showing thatsr was not less than about 10 d–1. The authors derived absorption parameter values of fr =0.02, sr = 10 d–1 and ss = 1x10–6 d–1, giving assignment to Type S. However, they consideredthat the value of fr should not be regarded as typical of ThO2. They referred to in vitro
dissolution tests (Lamont et al., 2001, see above) which showed much lower values of fr. In
view of this, specific parameter values are not adopted for thorium dioxide, which is assigned
to Type S, but it should be recognised that absorption could be even lower than assumed for
default Type S.
Thorium ore and refinery dusts(804) Measurements of thorium decay products in the chest and exhaled air of nearly 200
former thorium refinery workers, made three or more years after the end of exposure to arange of compounds from monazite ore to thorium nitrate, indicate long-term retention andhence Type S behaviour for at least some of the material (Stehney et al., 1980; Rundo et al.,1981). (See also the section below on decay products of thorium formed in the respiratory
tract.) Analysis of autopsy tissues from five workers showed excess concentrations ofthorium in lung and lymph nodes (Mausner 1982; Stehney and Lucas 2000). The authors
noted that the large amounts of 232Th remaining in the lungs 6–30 years after the end of
employment supported the long-term lung retention assumed in the original HRTM.
(805) Maniyan et al. (2000) carried out repeated in vivo measurements of the decay product208
Tl in the chest of four workers at a monazite processing plant. They had previous chronic
inhalation exposure for 25 to 30 years mainly to thorium hydroxide and phosphate.
Measurements, which extended over periods of ~500–1200 days, indicated a clearance halflife for thorium in the chest of ~1000 days. However it was recognised that because of thelong exposure there were contributions to the measurements from activity in lymph nodes andskeleton.
(806) Jaiswal et al. (2004) reported that the ratios of daily urinary excretion to lung content
of thorium in five workers exposed chronically (10–32 years) at a plant that processed
thorium concentrate (hydroxide) to produce thorium nitrate and oxide, were consistent withthe predictions of the HRTM and ICRP Publication 69 systemic Th model (ICRP 1994b;
1995a) assuming Type S, but not Type M.
(807) As part of a programme of measurements of the dissolution in simulated lung fluidof thorium and uranium in dusts to which workers were exposed (see below), Duport et al.
(1991) observed negligible dissolution of 232Th in samples of Ni-ThO2 (2%Th: 98%Ni) alloy
from a plant that produced heat and corrosion resistant alloys for aircraft industries.
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Uranium ore dust
(808) There is experimental evidence that thorium present in uranium ore dust is retainedin the lungs longer than other constituents of the particle matrix (Stuart and Beasley 1967;
Stuart and Jackson 1975). Similarly, Fisher et al. (1983) measured significantly higher
activity levels of 234U and 238U than of the decay product 230Th in excreta samples obtained
from active uranium millers, indicating that clearance of uranium in the inhaled ore dust was
faster than that of thorium. In contrast, Wrenn et al. (1985) measured 230Th concentrations
similar to those of 234U in the lungs of five uranium miners. In a later study (Singh et al.,1987) the same group found 230Th to 234U concentrations ratios >1 in the lungs of threeuranium miners and two uranium millers. They concluded that overall, dissolution in thehuman lungs of uranium and thorium in uranium ore dust was similar. For further
information see the section on decay products of uranium formed in the respiratory tract.
(809) Duport et al. (1991) measured the dissolution in simulated lung fluid of long lived
radionuclides in uranium ore dust from Canadian mines. (For further information see thesections on decay products of uranium and thorium formed in the respiratory tract). For highgrade ore, measurements were made for up to 60 days. Results were presented as undissolved
fractions as functions of time, and showed two components, which were expressed as Class D(rapid) and Class Y (slow) fractions. For 238U and 230Th, the rapidly dissolved fractions were0.25 and 0.15 respectively, indicating assignment to Type M. (HRTM parameter values fitted
to the 230Th data by Marsh et al., 2011, were: fr = 0.14, sr = 4.6 d–1 and ss = 0.0007 d–1). For
both radionuclides, no effects of size were observed in total dissolution over 40 days forparticles in size ranges 7–10, 3–7, 1–3 and <1 µm. For low grade and medium grade ores,measurements were made for 12 days, but only on samples of relatively coarse dust, thesmallest fraction being <37 µm. For 238U, rapidly dissolved fractions were greater than thosemeasured in the high grade ores: ~0.33 and 0.5 for low and medium grade ores respectively.
Measurements were also made of 232Th in low grade ore, and a much lower fraction obtained,
0.01, indicating assignment to Type S.
(810) Reif (1994) measured the dissolution rates in simulated lung fluid of thorium
residues from two different uranium mill tailings in the USA for 100 days. Dissolution
parameter values calculated were ss = 6.4x10-4 d–1 for one compound, and fr = 0.3, sr = 0.23 d–1
and ss = 4.1x10-3 d–1 for the second compound, indicating assignment to Type S and Type M
respectively.
(811) Bečková and Malátová (2008) measured dissolution for 26 days of 238U, 234U and230
Th in simulated serum ultrafiltrate of uranium ore dust collected on personal air filters in amine in the Czech Republic. The dust contained no measurable 232Th series radionuclides.
Moderate dissolution of both uranium isotopes was observed, indicating assignment to Type
M. (For further information see the uranium inhalation section.) In contrast no dissolution of230
Th was detected, indicating assignment to Type S.
Other mine dusts(812) Chen et al. (1995) followed lung retention of thorium by measurements of exhaledthoron in a worker involved in crushing ore containing iron, rare earths and thorium(~0.04%). This worker’s lung content was the highest found in a survey of over 100 workers
at the mine (Chen et al., 1988), and he suffered from pneumoconiosis. About 40% of thethorium remaining in the lungs when exposure stopped cleared within about a year, but there
was very little further clearance during the following 5 years, indicating Type S behaviour ofat least some of the dust.
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Environmental thorium(813) Although mainly related to public, rather than worker exposure, information relating
to environmental thorium is included here for completeness.
(814) Measurements of environmental levels of thorium in autopsy tissues from membersof the public showed that the fraction of thorium in the lungs (~25% of the estimated total
body content) was considerably greater than that of plutonium (~5%), and suggested a longterm lung retention half-time for thorium of between 1 and 8 y (Wrenn et al., 1981; Singh etal., 1983). The concentrations of thorium in the lymph nodes were 10-20 times those in thelungs in autopsy tissues from members of the public (Hamilton et al., 1972; Ibrahim et al.,
1983; Singh et al., 1983; Wrenn et al., 1985; Sunta et al., 1987).
(815) Jaiswal et al. (2004) found good agreement between measured values of Th in lung,skeleton and liver in autopsy tissues from members of the public, and those predicted by the
HRTM assuming Type S, and the ICRP Publication 69 systemic model for Th (ICRP 1994b;
1995a).
(816) These results indicate that environmental thorium is inhaled mainly in insoluble
forms.
Decay products of thorium formed in the lungs(817) The general approach to treatment of decay products formed in the respiratory tract
is described in Part 1, Section 3.2.3. In summary, it is expected that generally the rate at
which a particle dissociates is determined by its matrix, and hence the physico-chemical formof the inhaled material. It is recognised that for decay products formed within particles byalpha emission, recoil of the daughter nucleus from the alpha emission expels some of the
decay product from the particle. In the case of decay chains, this will result in successively
lower activities of members compared to the parent retained in relatively insoluble particles.
Experimental evidence relating to this is described below in the section on relatively insoluble
forms of thorium. However, it was considered impractical to implement loss of decay
products by alpha recoil in the calculation of dose coefficients and bioassay functions in thisseries of documents. (For further information see Part 1, Section 3.2.3.) Nevertheless, thisphenomenon should be borne in mind, especially when using decay products to monitor
intakes and doses of the parent. This is of particular importance in the case of thorium.
(818) Exceptions are made for noble gases formed as decay products, which are assumed
to escape from the body directly, in addition to other routes of removal. For calculation
purposes it is assumed that radon formed as a decay product within the respiratory tract
escapes from the body at a rate of 100 d–1, in addition to other routes of removal. For further
information see the section below on relatively insoluble forms of thorium.
(819) The decay schemes of thorium isotopes in the natural decay series: 227Th, 228Th,
230
Th, 231Th, 232Th and 234Th are shown in Part 1, Figures 3.9, 3.10, 3.11. The 232Th decay
series is also shown here and the 238U and 235U decay series are shown in the uranium
inhalation section.

269

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
Thorium-228

Thorium-232
α

14 billion years
ββRadium-228

α

1.9 years

6.1 hours

Actinium-228*

Notes:The symbols α and β indicate alpha and beta
decay, and the times shown are half-lives.

5.8 years

An asterisk indicates that the isotope is also
a significant gamma emitter.
Radium-224
α

3.7 days

Radon-220α

50 seconds

Polonium-216
αPolonium-212

0.15 seconds

βα61 minutes(64%)

310 nanoseconds

Bismuith-212*βα11 hours

61 minutes(36%)
Lead-208 (stable)

Lead-212*β

3.1 minutes

10751
10752
10753
10754
10755
10756
10757
10758
10759
10760
10761
10762
10763
10764
10765
10766
10767
10768
10769
10770
10771
10772
10773
10774
10775
10776
10777
10778
10779

Thallium-208*

Figure 14-1. Natural decay series: Thorium-232(820) It is expected that the behaviour of soluble (e.g. Type F) material in the respiratory
tract would depend on its elemental form, i.e. that of the decay product. Nevertheless, forsimplicity, in this series of documents the absorption parameter values of the parent are, by
default, applied to all members of the decay chain formed in the respiratory tract.
(821) The behaviour of decay products of thorium can be of particular importance in thiscontext, because there is generally significant long-term retention of thorium in the lungs
following its deposition in water-soluble form (see above). Conversely, soluble forms ofimportant decay products of thorium, notably radium and lead, are relatively readily absorbed
from the respiratory tract into the systemic circulation. Studies specifically comparing the
behaviour of thorium with that of its decay products are summarised below, although it
should be noted that the decay products were administered with the thorium as well as being
formed from decay of thorium (and its daughters) in the respiratory tract. For more
information, see also the sections on radium, lead, polonium, bismuth and uranium, relating
to the behaviour of their decay products formed in the respiratory tract.
(822) As noted above, measurements have been made of the tissue distributions of 212Pb,
212
Bi and 208Tl, following administration to rats of 228Th in various chemical forms (nitrate,hydroxide, fluoride, dioxide), in equilibrium with its decay products. (Radon-220 is aprecursor of 212Pb, but it is unlikely that a significant amount was lost from solution before
deposition in the lungs, because of its short half life of 56 seconds. Its average half-distanceof diffusion in water was estimated to be 50 µm by Ballou and Hursh, 1972.) The behaviourof 212Pb is compared with that of 228Th for each chemical form below. (For further
information see the lead inhalation section.) In all these studies the distributions of 212Bi and208
Tl were similar to each other and those of the parent 212Pb. Because their physical halflives are so short (61 minutes and 3 minutes respectively) measurements made at 6 hours
onwards would be mainly of activity formed from decay of 212Pb within the body, rather than270

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10780
10781
10782
10783
10784
10785
10786
10787
10788
10789
10790
10791
10792
10793
10794
10795
10796
10797
10798
10799
10800
10801
10802
10803
10804
10805
10806
10807
10808
10809
10810
10811
10812
10813
10814
10815
10816
10817
10818
10819
10820
10821
10822
10823
10824
10825
10826
10827

from intake of 212Bi or 208Tl. The similar distributions of 212Bi and 208Tl to those of 212Pb
might suggest that there was not rapid movement of 212Bi from the site (e.g. the lungs) inwhich it was formed by decay of 212Pb. However, 212Bi (and 208Tl) would have grown in
rapidly between dissection of the animals and measurements of activities in tissues. Thus theactivities of 212Bi (and 208Tl) present in vivo, may have been significantly lower than thosemeasured and without detailed information (which is not available) about the time which
elapsed between dissection of the animals and measurements, it is not possible to correct forthis ingrowth and hence estimate the absorption rate from the respiratory tract of the bismuth
formed as a decay product of lead, nor that of the thallium formed as a decay product ofbismuth. However, since the half-life of 208Tl is so short (as is that of 207Tl present in the 235U
decay series, 5 minutes), the absorption rate would have to be very high to influence dose
assessments.
Relatively soluble (Type M) forms(823) Ballou et al. (1986) measured the tissue distributions of 232U, 228Th, 224Ra, 212Pb,
212
Bi and 208Tl at 24 hours after intratracheal instillation into rats of 232U nitrate with its decay
products. (For further information see the uranium inhalation section.) Measurements of
228
Th, 224Ra, and perhaps 212Pb, were mainly of material administered with the parent 232U,
rather than formed from its decay in the lungs. The physical half-lives of 212Bi and 208Tl are soshort, 61 minutes and 3 minutes respectively, that measurements made at 24 hours would
mainly be of activity formed in situ. Lung retention was 7.9% ILD for 232U, 52% ILD for
228
Th, and about 2-3% ILD for the other decay products measured, reflecting the high lungretention of thorium, and relatively rapid lung clearance of radium and lead observed in otherstudies in which soluble forms were administered. Similarly, the distribution between liver,skeleton and kidneys of 232U, 228Th, 224Ra and 212Pb reflected the elemental forms. The
distributions of 212Bi and 208Tl were similar to those of 212Pb, presumably because of theirshort physical half-lives: whatever their distribution in vivo, they would tend to equilibrium
between dissection and measurement.
(824) Lipsztein et al. (1989) made in vivo measurements of 228Ac and 208Tl in the lungs of
two workers involved in the chemical treatment of monazite sand. They considered that the
exposures were to “Class W” (moderately soluble i.e. Type M) forms of thorium. The mean
ratio of 228Ac to 208Tl was 1.5, suggesting that some members of the decay series cleared
faster than the 228Ac, but the differences were not great.
(825) Moody et al. (1994a; Moody and Stradling, 1992) measured the tissue distributionsof 228Th, 212Pb, 212Bi and 208Tl, at times from 6 hours to 7 days after intratracheal instillation
into rats of a solution of 228Th nitrate in equilibrium with its decay products. For 228Th, on
average 48% ILD was measured in the lungs at 6 hours and 40% ILD at 1 day (see above).
For 212Pb, clearance was much faster, with 8.4% ILD at 6 hours and 1.2% ILD at 1 day(correcting for the physical decay of 212Pb, 12.5% and 5.6% ILD respectively). Latermeasurements of 212Pb could have included significant ingrowth of 212Pb from decay ofhigher members of the chain in the lungs. Nevertheless the concentration of 212Pb remainedmuch lower than that of the 228Th parent, (presented as a high 228Th:212Pb ratio).
(826) Stradling et al. (2005b; Moody et al., 1994b) measured the tissue distributions of
228
Th, 212Pb, 212Bi and 208Tl, at times from 1 to 168 days after intratracheal instillation into
rats of a suspension of 228Th or 228+232Th fluoride in equilibrium with the decay products of228
Th. For thorium (see above), on average 65% ILD was measured in the lungs at 1 day
when administered with a low mass (60 pg) of thorium, and 72% ILD when administeredwith a high mass (6.5 µg) of thorium. For 212Pb, the corresponding amounts were 6.0% and271

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10828
10829
10830
10831
10832
10833
10834
10835
10836
10837
10838
10839
10840
10841
10842
10843
10844
10845
10846
10847
10848
10849
10850
10851
10852
10853
10854
10855
10856
10857
10858
10859
10860
10861
10862
10863
10864
10865

18% ILD. Correcting for the physical decay of 212Pb gives retention of 28% and 84% ILD at 1day. Thus, at the low mass, clearance was much faster than that of the parent 228Th, but not at
the high mass. From the results for low mass it was assessed here that sr was at least 1 d–1(half-time ~8 hours). Later measurements of 212Pb could have included significant ingrowthof 212Pb from decay of higher members of the chain in the lungs. Nevertheless, as for thenitrate, the concentration of 212Pb remained lower than that of the 228Th parent, (presented asa high 228Th:212Pb ratio).
(827) Stradling et al. (2005b; Moody et al., 1994b) measured the tissue distributions of
228
Th, 212Pb, 212Bi and 208Tl, at times from 1 to 168 days after intratracheal instillation into
rats of a suspension of 228Th or 228+232Th hydroxide in equilibrium with the decay products of228
Th. For thorium (see above), on average 59% ILD was measured in the lungs at 1 day
when administered with a low mass (60 pg) of thorium, and 75% ILD when administeredwith a high mass (6.5 µg) of thorium. For 212Pb, the corresponding amounts were 2.7% and5.3% ILD. Correcting for the physical decay of 212Pb gives retention of 13% and 25% ILD at
1 day. At both mass levels clearance of 212Pb was much faster than that of the parent 228Th.
Later measurements of 212Pb could have included significant ingrowth of 212Pb from decay ofhigher members of the chain in the lungs.
(828) In the studies by Moody et al. (1994a; 1994b), Moody and Stradling, (1992) andStradling et al. (2005b) the concentration of 212Pb remained much lower than that of the 228Th
parent, despite ingrowth (presented as a high 228Th:212Pb ratio). This might be partly due toloss of intermediate decay products by alpha recoil and diffusion of radon, but partly also due
to more rapid dissolution (leaching) of the decay products, including 212Pb, from the particle
matrix. Stradling et al. (2004) proposed that since the decay products (radium and lead) are
rapidly absorbed, as expected for radium and lead nitrates, they should be assigned to Type F.
(829) For the other moderately soluble forms the situation is less clear: retention of lead isless than that of thorium, but greater than that of lead nitrate. The decay products are
therefore also assigned to Type M.
Relatively insoluble (Type S) forms(830) As noted above (section on Uranium ore dust), Duport et al. (1991) measured thedissolution in simulated lung fluid of long lived radionuclides in uranium ore. For high gradeore, measurements were made for up to 60 days, on particles in size ranges that included
respirable particles. Results were presented as undissolved fractions as functions of time, andshowed two components, which were expressed as Class D (rapid) and Class Y (slow)
fractions. For 238U, 230Th, 226Ra, and 210Pb, the rapidly dissolved fractions were 0.25, 0.15,
0.12 and 0.28 respectively. Marsh et al., 2011, fitted two-component exponential functions to
the data (un-dissolved fractions) and obtained the following HRTM parameter values:
Nuclide
230
Th
226
Ra
210
Pb

10866
10867
10868
10869
10870
10871

fr
0.14
0.11
0.26

sr (d–1)
4.6
7.3
3.9

ss (d–1)
0.00070.00040.001(831) For these radionuclides, no effects of size were observed in total dissolution over 40days for particles in size ranges 7–10, 3–7, 1–3 and <1 µm. For low grade and medium gradeores, measurements were made for 12 days, but only on samples of relatively coarse dust, thesmallest fraction being <37 µm. For 238U, rapidly dissolved fractions were higher (0.33 and
0.5 for low and medium grade ores) than those measured in the high grade ores. However, for272

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10872
10873
10874
10875
10876
10877
10878
10879
10880
10881
10882
10883
10884
10885
10886
10887
10888
10889
10890
10891
10892
10893
10894
10895
10896
10897
10898
10899
10900
10901
10902
10903
10904
10905
10906
10907
10908
10909
10910
10911
10912
10913
10914
10915
10916
10917
10918
10919

other radionuclides the fractions were lower: 0.07 for 226Ra, and <0.01 for 210Pb.
Measurements were also made for 210Po in low and medium grade ores, and low fractions
obtained, 0.00 and 0.005 respectively. Consistent differences in dissolution between uranium,
thorium and their decay products were not apparent.
Emanation of radon: recoil and diffusion(832) Griffiths et al. (1980) developed a model to describe the retention of 232U and its
decay products, which include 228Th, in the lungs following inhalation in ThO2 or UO2
particles. In addition to chemical dissolution, they considered recoil emanation of daughter
product nuclei by alpha-particle decay, and diffusion emanation of 220Rn from particles. They
presented equations to calculate fractional losses by recoil and diffusion as functions ofparticle size (but only for spherical particles). They calculated recoil ranges of about 0.05 µm
for the decay products, assuming a particle density of 10 g cm–3, and fractional losses byrecoil emanation in the range 0.3 – 0.1, for aerosols with AMAD in the range 1 – 10 µm. The
calculated loss of 220Rn from particles by diffusion emanation was difficult to predict, ranging
from 0.03 to 0.7 depending on the assumed diffusion coefficient (10–15 - 10–11 cm2 s–1).
(833) Coombs and Cuddihy (1983) measured the fraction of 228Th escaping by recoil andthe fraction of 220Rn escaping by diffusion from size-fractionated samples of ThO2 anduranium oxide (mixture of UO2.2 and U3O8) containing 1% 232U. The fraction of 228Th
escaping increased from ~0.07 for particles with AMAD 2.5 µm (count median diameter,
CMD ~1 µm) to ~0.3 for particles with AMAD 0.65 µm (CMD ~0.1 µm). This was inreasonable agreement with the model of Griffiths et al. (1980). Calculated recoil range wasexpressed in terms of recoil range times density, with values of ~20 µg cm–2. The fraction of220
Rn escaping by diffusion increased from ~0.07 for particles with AMAD 2.5 µm, to ~0.35
for particles with AMAD 0.65 µm, and gave a diffusion coefficient of ~3x10–14 cm2 s–1. Thiswas similar to the fraction of 228Th escaping by recoil, and therefore presumably similar to thefraction of 220Rn escaping by recoil, since the recoil ranges of 220Rn and 228Th are similar(Griffiths et al., 1980).
(834) Johnson and Peterman (1984) developed a model to describe the emanation of 220Rn
from ThO2 particles by alpha-particle recoil, and its exhalation from the lungs. They
calculated that the fraction of 220Rn atoms produced that escaped from particles (density 10 gcm–3) by recoil decreased from ~1.0 at 1 nm to ~0.5 at 10 nm and ~0.1 at 0.5 µm diameter.
The average fraction for an aerosol of AMAD 1 µm was calculated to be 0.2, which seems to
be consistent with the results derived by Griffiths et al. (1980).
(835) Ballou and Hursh (1972) measured thoron (220Rn) in the breath of dogs at times up
to 150 days after inhalation of ThO2 (see above) and, for comparison, after intravenous
injection of ThO2. (After intravenous injection, about 75% of the ThO2 was retained in thelung vasculature.) Lung retention of 228Th was also followed by in vivo measurements of 208Tl
gamma emissions over the thorax, and post mortem measurements of 228Th in the lungs. At
14 days, the activity of the 224Ra daughter was about 70% of that of the 228Th, suggestingsome differential loss of 224Ra. The ratio of thoron in the lung space to 228Th in the wholebody was lower (0.065) immediately after inhalation than after intravenous injection (0.11),
but increased to about 0.1 by 14 days. By this time most of the 228Th was in the lungs, andthe ratio of thoron in the lung space to 228Th in the lungs remained fairly constant thereafter.
The lower initial value was attributed to the particles’ being embedded in mucus in the upper
respiratory tract.
(836) Measurements of thorium decay products in the chest (212Bi, and in some cases
228Ac) and exhaled air (thoron, 220Rn) of nearly 200 former thorium refinery workers, were273

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10920
10921
10922
10923
10924
10925
10926
10927
10928
10929
10930
10931
10932
10933
10934
10935
10936
10937
10938
10939
10940
10941
10942
10943
10944
10945
10946
10947
10948
10949
10950
10951
10952
10953
10954
10955
10956
10957
10958
10959
10960
10961
10962
10963
10964
10965
10966
10967

made three or more years after the end of exposure to a range of compounds from monazite
ore to thorium nitrate (Stehney et al., 1980; Rundo et al., 1981; Toohey et al., 1985).
Measurements of exhaled thoron were expressed as the activity of freely emanating 224Ra (theparent of 220Rn) at the mouth of the subject. They found an average value of 0.101 for theratio of freely emanating 224Ra to retained 212Bi, from which they deduced an average
exhalation of 9.2% of the thoron produced. Stebbings (1985) reported a positive correlation
between this ratio and the thorium body content, which could lead to serious underestimation
if it were applied to estimate the thorium body content from exhaled thoron at population
exposure levels.
(837) Rundo and Toohey (1986) reported that measurements of 212Bi in the thorax and of
exhaled thoron made on an employee of a ceramics firm showed no change over a period of 7
years. Mean values reported gave a value of 0.07 for the ratio of freely emanating 224Ra toretained 212Bi, similar to that reported by Rundo et al. (1981) for former thorium refinery
workers.
(838) Terry and Hewson (1993, 1995) measured thoron in the breath of 62 workers
exposed to monazite dust in the mineral sands industry. For 6 of them, in vivo measurements
were also made of 228Ac, 212Pb and 208Tl in the lungs. The authors estimated that on average
4.7% of the thoron produced in the lungs was exhaled. They also reported that (excluding
data for the two workers with the lowest lung burdens) the mean ratio of the 911 keV 228Ac
peak to the 2,615 keV 208Tl peak was 1.42. They inferred that the 232Th decay series is not in
secular equilibrium, but that up to 30% of the decay products formed from 228Ac to 208Tl had
translocated from the lungs.
(839) Hodgson et al. (2000, 2003) measured the tissue distributions of 228Th, 212Pb, 212Bi
and 208Tl, at times from 1 to 168 days after intratracheal instillation into rats of suspensions of
232
Th dioxide enriched with 228Th in equilibrium with its decay products, with geometricdiameters of about 0.4 and 2 µm. There was little absorption of the thorium itself, consistent
with assignment to Type S (see thorium dioxide section above). The activity of 212Pb in thelungs was about 50% and 80% of that of the thorium at 1 day for the 0.4 and 2 µm particles
respectively, and 25% and 70% at later times. The lower concentrations of 212Pb were
attributed to diffusion of 220Rn (thoron) and recoil of the progeny from alpha particle decay,
and the authors suggested that the concentration of 212Pb relative to that of 228Th would beeven lower following deposition of ultrafine particles. These inferences are consistent withthe conclusions of Coombs and Cuddihy, 1983 (see above), although some more rapid
dissolution of lead (and/or its precursors) than of thorium cannot be completely excluded.
(840) Thus, consideration of the recoil range of decay product nuclei formed by alphaemission and measurements of emanation of such decay products indicate that an important
fraction is transferred from particles to the surrounding medium. Measurements of decay
product ratios to thorium seem broadly consistent with this model. The fraction decreases
with increasing particle size and density, but is of the order of 10% for aerosols likely to be
encountered in the workplace. However, as noted above, it was considered impractical to
implement loss of decay products by alpha recoil in the calculation of dose coefficients andbioassay functions in this series of documents. (For further information see Part 1, Section
3.2.3.) Nevertheless, this phenomenon should be borne in mind, especially when using decay
products to monitor intakes and doses of thorium.
(841) For calculation purposes it is assumed that radon formed as a decay product within
the respiratory tract escapes from the body at a rate of 100 d–1, in addition to other routes ofremoval (ICRP, 1995b). This rate was set as a convenient, arbitrary, rapid rate. The
underlying assumption is that loss of radon is a continuous process such as diffusion. The
274

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
10968
10969
10970
10971
10972
10973
10974
10975
10976
10977
10978
10979
10980
10981
10982
10983
10984
10985
10986
10987
10988
10989
10990
10991
10992
10993
10994
10995
10996
10997
10998
10999
11000
11001
11002
11003
11004
11005
11006

three radon isotopes in the natural decay series: 222Rn (radon), 220Rn (thoron), and 219Rn(actinon) have half-lives of about 3.8 days, 56 seconds and 4 seconds, and therefore decay
rates of about 0.18, 1100 and 15,000 d–1, respectively. Hence the assumption of a rate of lossof 100 d–1 implies that nearly all 222Rn escapes from the particles before it decays, about 10%
of 220Rn escapes, and nearly all 219Rn decays within the particles.
(842) The predicted transfer to lung air of ~10% of 220Rn formed is broadly consistent withobservations that ~10% of the thoron produced in particles in the lungs is exhaled (seeabove). It was assessed here that most of the 220Rn entering lung air is exhaled 3. However, theprediction that all of the 222Rn escapes from the particles is not supported by measurements ofradon emanation coefficients (the fraction of radon atoms that escape from the particles inwhich they were formed) made on dust samples. Duport and Edwardson (1984) reported
values between 0 and 0.5 for micron sized samples of uranium ore dust. Kalkwarf et al.
(1985) measured radon emanation coefficients in the range 0.001 to 0.1 for coal fly ash
particles in sized fractions from <0.5 µm to 11-15 µm. They recognized that since theparticles in their experiments were closely packed, some recoiling radon would be injected
into adjacent particles, and emanation would be somewhat greater in the lungs. Strong andLevins (1982) measured the effect of moisture content on emanation of radon from uranium
mine tailings. The radon flux from a column of powder was higher when it was moist thanwhen it was dry: this was attributed to recoiling radon atoms being stopped in the water
between particles (from which it subsequently diffused) rather than becoming trapped in otherparticles. The discussion assumed that the main mechanism of radon loss from particles wasrecoil following decay of the parent 226Ra. Thus the assumption of a rate of transfer of radonfrom particles of 100 d–1 appears to be pragmatic: it is simply to apply and seems to predictexhalation of 220Rn (thoron) in broad agreement with observations, but probably
overestimates loss of 222Rn from particles in the lungs.
Rapid dissolution rate for thorium(843) In the various studies of the biokinetics following deposition in the lungs of watersoluble forms of thorium it was observed that only a fraction of the ILD, usually less than
50%, was absorbed into blood, and that most of the absorption had taken place by the time of
the first measurement of tissue distribution. The earliest measurements of distribution weremade <1 hour after inhalation of thorium chloride or citrate by rats, which indicated that theabsorption rate corresponds to a time constant of less than an hour, i.e. that sr was more than
20 d–1. However, it was not very much greater, because it appeared that clearance from theupper respiratory tract was mainly to the alimentary tract. Values of fr estimated here fromthe results of three experiments were 20, 70 and 90 d–1. A central value of 50 d–1 is adopted
here, and applied to all Type F forms of thorium. However, as noted in the introduction
above, the results of studies of water-soluble forms of thorium (chloride, citrate, nitrate,sulphate) deposited in the lungs, indicate that there are no commonly encountered Type F
3

According to Stehney et al. (1980) the average breathing rate during measurements of thoron in breath was 7.5
litres per minute. An adult male at rest takes about 12 breaths per minute (ICRP 1994c, page 194): hence thetidal volume was ~0.6 litres and each breath took ~5 seconds. The volume of air in the lungs at the start of abreath is ~3.9 litres (Functional Residual Capacity, 3.3 litres (ICRP 1994c, page 189) plus tidal volume 0.6
litres). Hence ~15% of the air in the lungs is exhaled, and it is assumed here that a similar proportion of thethoron is exhaled. During the 5 seconds of a breathing cycle, ~6% of the thoron present decays, and hence any
thoron atom is ~2.5 times more likely to be exhaled than to decay during this breath, or any other. This is in
broad agreement with Johnson and Peterman (1984), who calculated that the proportion of 220Rn atoms enteringlung air that was exhaled increased from ~60% in airway generations >20 to ~80% in airway generations <16.

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DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
11007
11008
11009
11010
11011
11012
11013
11014
11015
11016
11017
11018
11019

forms of thorium.
Extent of binding of thorium to the respiratory tract(844) As noted above, in the various studies of the biokinetics following deposition in thelungs of water soluble forms of thorium it was observed that only a fraction of the ILD,
usually less than 50%, was absorbed into blood. Clearance from the lungs continued, withexcretion mainly to faeces, indicating that the clearance was predominantly by particle
transport, and that the thorium was retained in the lungs in particulate form, rather than in thebound state. Adequate fits to data were obtained here on that assumption. It is therefore
assumed that for thorium the bound state can be neglected, i.e. fb = 0.0.
Table 14-2. Absorption parameter values for inhaled and ingested thorium
Absorption parameter valuesa
Inhaled particulate materials
frSpecific parameter valuesc
Water soluble forms, including thorium 0.1
chloride, citrate, nitrate and sulphate;thorium fluorided
Default parameter valuese
Absorption
Assigned forms
TypeF— NB: Type F should not 1
beassumedwithout
evidence
Mf
Thorium hydroxide
0.2
Sf
Oxide,
allunspecified 0.01
formsgIngested material
All forms

11020
11021
11022
11023
11024
11025
11026
11027
11028
11029
11030
11031
11032
11033
11034
11035
11036
11037
11038

sr (d–1)

ss (d–1)

Absorption fromthealimentarytract, fAb

50

0.005

5 x 10–550-

5 x 10–4

3
3

0.005
1x10-41 x 10–4
5 x 10–6

5 x 10–4a

It is assumed that for thorium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F formsof thorium (50 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
b
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the (rounded) product of fA for theabsorption Type (or specific value where given) and the fA value for ingested soluble forms of thorium (5 x
10–4).
c
See text for summary of information on which parameter values are based, and on ranges of parameter values
observed for individual materials. For water soluble forms of thorium specific parameter values are used for
dissolution in the lungs, but the default value of fA.
d
Decay products assigned to Type F.
eMaterials (e.g. thorium hydroxide) are listed here where there is sufficient information to assign to a default
absorption Type, but not to give specific parameter values (see text).
f
Decay products assigned to Type M.
gDefault Type S is recommended for use in the absence of specific information, i.e. if the form is unknown, or
if the form is known but there is no information available on the absorption of that form from the respiratory
tract.

14.2.2. Ingestion

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11039
11040
11041
11042
11043
11044
11045
11046
11047
11048
11049
11050
11051
11052
11053
11054
11055
11056
11057
11058
11059
11060
11061
11062
11063
11064
11065
11066
11067
11068
11069
11070
11071
11072
11073
11074
11075
11076
11077
11078
11079
11080
11081
11082
11083
11084
11085
11086

(845) Maletskos et al. (1969) measured the absorption of 234Th ingested as the sulphate ina mock "dial" paint by six elderly humans. The values obtained were in the range 10-4 to
6.10-4 with a mean of 2.10-4. Estimates of Th absorption have also been derived by Johnson
and Lamothe (1989) from human data on skeletal content, dietary intake, estimated inhalation
rates and excretion data, giving values of less than 10-3 to 10-2. However, these estimates ofabsorption are uncertain because they are based on balance studies involving disparate data
sources. Dang and Sunta (1992) questioned the higher uptake values reported by Johnson andLamothe (1989) and reinterpreted the data used by them to suggest absorption values of about
10-3 - 2x10-3. Their own data for Th concentrations in tissues, body fluids, and daily diet for
urban Indian populations suggested values lower than 10-3. Roth et al. (2005) measured
urinary excretion of 232Th in 11 adults who were not occupationally exposed. Comparison
with reference intake values suggested that absorption was around 5 x 10-3.
(846) There have been several reports of Th absorption in rats and mice, with values of
5.10-5 to 6.10-3 for rats (Traikovich, 1970; Pavlovskaya et al, 1971; Sullivan, 1980), about
6.10-4 for mice (Sullivan, 1980; Sullivan et al., 1983) and 1.10-3 for fasted mice (Larsen et al.,1984).
(847) In Publication 30 (ICRP, 1979), an absorption value of 2x10-4 was recommended on
the basis of the study of Maletskos et al. (1969). In Publication 67 (1993) and 69 (1994a),
because similar values have been obtained in more recent human studies on the absorption of
Pu, Am, Np and Cm, a general absorption value of 5x10-4 was adopted for dietary intake byadults for all actinides other than uranium. In Publication 68 (1994b), a value of 2x10-4 wasapplied to oxides and hydroxides, with 5x10-4 for all other chemical forms. An fA of 5x10-4 isadopted here for all chemical forms.
14.2.3. Systemic distribution, Retention and Excretion
14.2.3.1. Summary of the database
Human subjects(848) Maletskos et al. (1966, 1969) examined the clearance of thorium from blood and its
retention and excretion after intravenous injection of 234Th citrate into normal human subjectsof age 63-83 y. Detailed measurements were reported for 3 male and 2 female subjects(Maletskos et al., 1966). During the first day, thorium disappeared from blood with ahalf-time of a few hours. As an average, about 10% of the injected amount remained in blood
after 1 d, 3% after 2 d, 1.5% after 3 d, and 0.3% after 10 d. As indicated by whole-bodycounting and analysis of excreta, whole-body retention was greater than 90% of the injectedamount at 3 wk after injection. Cumulative urinary excretion represented 4.5-6.1% of theinjected amount over the first 5 d after injection and an additional 2-3% over the next 19 d.
Little activity was lost in faeces during the first five days. The ratio of urinary to faecal
excretion over the first five days averaged about 12 for the male subjects and 25 for thefemale subjects. External measurements indicated virtually no biological removal from thebody during the period from 3-16 wk after injection. There appeared to be no disproportionate
accumulation of thorium in the liver compared with other soft tissues.
(849) Long-term measurements of 227Th or 228Th in the bodies and excreta of accidentally
exposed workers suggest a minimum biological half-time of 10-15 y for the total-bodycontent (Rundo, 1964; Newton et al., 1981). Similar measurements on workers chronically
exposed to thorium over 1-3 decades (Dang et al., 1992) suggest that the rate of removal of
the systemic burden to urine was less than 1% y-1.
277

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11091
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11093
11094
11095
11096
11097
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11099
11100
11101
11102
11103
11104
11105
11106
11107
11108
11109
11110
11111
11112
11113
11114
11115
11116
11117
11118
11119
11120
11121
11122
11123
11124
11125
11126
11127
11128
11129
11130
11131
11132
11133
11134

(850) Stehney and Lucas (2000) reported concentrations of 232Th and activity ratios of
228
Th to 232Th and 230Th to 232Th in autopsy samples from five subjects who had worked for
3-24 y at a thorium refinery. Times from the end of work to death ranged from 6 to 31 y. The
subjects presumably were exposed primarily by inhalation. For three workers for whom
analyses were available for both bone and liver, the 232Th content of total bone averaged
roughly 20 times that of the liver based on reference organs masses. For two workers forwhom analyses were available for both liver and kidney, the 232Th content of the liver
averaged roughly 30 times that of the kidneys. In most samples the activity ratios 228Th:232Th
and 230Th:232Th were in the ranges 0.2-0.4 and 0.1-0.2, respectively.
(851) Measurements of thorium isotopes in autopsy samples from non-occupationally
exposed subjects (Wrenn et al., 1981; Singh et al., 1983; Ibrahim et al., 1983) indicate that theskeleton typically contains more than three-fourths of the systemic burden during or after
chronic exposure to thorium. The reported contents of the liver and kidneys are variable but
typically represent about 2-4% and 0.3-1%, respectively, of the systemic burden. Theseestimates are based on the assumption that muscle, fat, and skin do not accumulate more than
20% of the systemic content, as suggested by data on laboratory animals (Stover et al., 1960;
Thomas et al., 1963; Boecker et al., 1963; Traikovich, 1970; Larsen et al., 1984).
(852) Glover et al. (2001) reported detailed measurements of 232Th in tissues of a wholebody donor to the United States Transuranium and Uranium Registries. The subject had no
known occupational exposure to thorium but had occupational intakes of plutonium andamericium and had been chelated with DTPA following an incident 19 years before his death.
The authors estimated that the skeleton, liver, kidneys, and other soft tissues contained about
56%, 0.36%, 0.19%, and 43% of systemic 232Th. The ratio 156 of skeletal 232Th to liver 232Th
estimated for this subject is substantially greater than values typically determined for humansubjects with or without occupational exposure to 232Th.
Laboratory animals(853) Stover et al. (1960) studied the biological behavior of 228Th in adult beagle dogs overa 1300-d period following its intravenous administration. Biological retention was about
88% of the injected amount at 3 wk, 80-85% at 3 mo, and 65-70% at 2.5 y (Fig. 5). The
urinary excretion rate was about 4 times the faecal excretion rate in the first few weeks, but
the urinary-to-faecal excretion ratio gradually decreased and was close to 1 at 2.5 y after
injection. About 70%, 5%, and 3% of injected thorium deposited in the skeleton, liver, andkidneys, respectively. At times greater than 100 d after administration, about 80% of retained
thorium was in the skeleton and about 20% was widely distributed in soft tissues, withrelatively high concentrations in the liver and kidneys. There was little if any decline in thethorium content of compact bone over 1300 d or in trabecular bone over 800 d, but there wasa noticeable decline in activity in trabecular bone over 800-1300 d after administration. The
thorium content of the liver and kidneys declined considerably in the first several months
after injection but showed little or no decrease thereafter. Retention of thorium in the kidneys
and its rate of urinary excretion at times remote from injection may have been affected byradiation damage at high dosage levels (Stover et al., 1960).
(854) Comparison of the organ distributions of thorium isotopes in humans and beagles
exposed only to environmental levels indicate broad similarities in the long-term distributionsof systemic thorium in the two species (Singh et al., 1988). There are also broad similarities
in the patterns of distribution and excretion of injected thorium in human subjects (Maletskos
et al., 1966, 1969) and beagles (Stover et al., 1960) at early times after administration.
(855) The biokinetics of systemic thorium has been studied in various small mammals
278

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11136
11137
11138
11139
11140
11141
11142
11143
11144
11145
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11147
11148
11149
11150
11151
11152
11153
11154
11155
11156
11157
11158
11159
11160
11161
11162
11163
11164
11165
11166
11167
11168
11169
11170
11171
11172
11173
11174
11175
11176
11177
11178
11179
11180
11181
11182

including rats, mice, guinea pigs, and rabbits (Scott et al., 1952; Thomas et al., 1963; Boecker
et al., 1963; Traikovich, 1970; Larsen et al., 1984). In many cases, the administration of highconcentrations of thorium apparently resulted in colloid formation and high deposition in thereticuloendothelial system or in the tissue into which thorium was introduced (e.g. lung withintratracheal injection, or muscle with intramuscular injection). The results of such high-dosestudies do not appear to be useful for determining the biokinetics of thorium after intake atlevels likely to be encountered in the environment or in most occupational situations.
(856) For tracer levels of thorium administered as the citrate to rats, deposition wasconsiderably greater in bone than other systemic tissues (Thomas et al., 1963). Muscle andpelt accounted for about 20% of the systemic activity at 7-54 d post injection.
(857) Boecker et al. (1963) found that the level of absorption of thorium to blood and its
subsequent pattern of distribution and excretion following acute inhalation by rats did notdepend on the initial lung content of inhaled thorium. The absorbed activity was deposited
mainly in the skeleton. The liver content at 0-40 d was about 15-20% of the skeletal content,
and the kidney content during that time was about 3% of the skeletal content. The content ofpelt and muscle plus connective tissue was about the same as liver. The urinary to faecal
excretion ratio increased gradually to a value of about 0.6-0.7 at 40-50 d post inhalation.
(858) At 3 d after injection of thorium into mice, about 90% of the systemic burden was
found in the skeleton, 6% in liver, 4% in kidneys, and 0.1% in reproductive organs (Larsen etal., 1984). A urinary to faecal excretion ratio of 16 was observed. The systemic distributionof thorium was essentially the same after gastrointestinal absorption as after intravenous
injection.
14.2.3.2. Biokinetic model for systemic thorium(859) The biokinetic model for systemic thorium used in this report is the model applied toadult members of the public in ICRP Publication 69 (1995a) and to workers in Publication 68(1994). The model structure (Figure 14-1) is the generic structure for bone-surface-seeking
radionuclides. Parameter values for a reference worker are listed in Table 14-3. The primaryparameter values such as compartment deposition fractions and biological half-times
underlying the transfer coefficients given in Table 14-3 are summarized below. The
conceptual basis of the model and the selection of parameter values are described by Leggett(1997).
(860) In the following summary of the model, the "removal half-time" from a compartment
refers to the biological half-time that would be observed if there were no recycling to thatcompartment. This will generally differ from the apparent or “externally viewed” half-timeobserved in the presence of recycling. Transfer coefficients from blood to various
compartments are based on "deposition fractions", which provide a convenient way todescribe the initial distribution of activity leaving the circulation.
(861) Blood is treated as a uniformly mixed pool. Compartment ST0 is a soft-tissue poolthat includes the extracellular fluids and exchanges material with blood over a period of days.
Compartment ST0 is used to depict an early build-up and decline of material in soft tissues
and to account for early feedback of material to blood. Compartment ST0 is viewed as anintegral part of the early circulation of thorium. In the summary of parameter values below,
deposition fractions for compartments other than ST0 are given in terms of activity “leaving
the circulation" and refer to the division of thorium among compartments other than ST0.

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11183

11184
11185
11186
11187
11188
11189
11190
11191
11192
11193
11194
11195
11196
11197
11198
11199
11200
11201
11202
11203
11204
11205
11206
11207
11208
11209

Figure 14-2. Structure of the biokinetic model for systemic thorium.

(862) The removal half-time from blood is assumed to be 0.25 d, corresponding to a totaltransfer coefficient (the sum of transfer coefficients to all repositories) of ln 2/0.25 d = 2.7726
d-1, where ln 2 is the natural logarithm of 2. Since 30% of this goes to ST0, the transfer
coefficient from blood to ST0 is 0.3 x 2.7726 d-1 = 0.8318 d-1. Transfer coefficients fromblood to other compartments are based on deposition fractions described below and the rate at
which thorium leaves the circulation, which is taken to be the total transfer coefficient fromblood to all compartments minus the transfer coefficient from blood to ST0: 2.7726 d-1 –0.8318 d-1 = 1.9408 d-1. For example, the transfer coefficient from blood to a compartment
with a deposition fraction of 0.01 is 0.01 x 1.9408 d-1 = 0.019408 d-1, before rounding.
(863) It is assumed that 70% of thorium leaving the circulation deposits on bone surface.
One-half of the deposited amount is assigned to trabecular surface and one-half is assigned tocortical surface. The fate of thorium after its deposition on bone surface is described by thegeneric model for bone-surface-seeking radionuclides. That is, the rate of translocation ofskeletal deposits is controlled by bone restructuring processes. The transfer coefficient fromcompact or trabecular bone surface or volume to the corresponding bone marrowcompartment is the rate at which that type of bone surface is resorbed. The transfer
coefficient from a bone surface compartment to the corresponding bone volume compartment
is one-half the surface formation rate. A common rate (referred to as the “bone turnoverrate”) is used for both bone formation and bone resorption and is applied both to surface andvolume remodeling. Bone turnover rates used here are reference values for adults given in
ICRP Publication 89 (2002). The removal half-time from bone marrow to blood is assumed
to be 0.25 y.

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11210

Table 14-3. Transfer coefficients in the biokinetic model for systemic thorium

From
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Liver 1
Liver 1
Liver 1
Cortical bone surface
Cortical bone surface
Trabecular bone surface
Trabecular bone surface
Kidneys 1a
Kidneys 2b
TestesOvaries
ST0
ST1
ST2
Liver 2
Cortical bone marrow
Cortical bone volume
Red marrow
Trabecular bone volume
a

b

11211
11212
11213
11214
11215
11216
11217
11218
11219
11220
11221
11222
11223

To
Liver 1
Cortical bone surface
Trabecular bone surface
Urinary bladder contents
Kidneys 1a
Kidneys 2b
Right colon contents
TestesOvaries
ST0
ST1
ST2
Blood
Liver 2
Small intestine contents
Cortical bone marrow
Cortical bone volume
Red marrow
Trabecular bone volume
Urinary bladder contents
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Blood
Cortical bone marrow
Blood
Red marrow

Transfer coefficient
(d-1)
0.097
0.67930.67930.10670.06790.01940.00970.000680.000210.832
0.243
0.03880.000475
0.00095
0.000475
0.0000821
0.0000411
0.000493
0.000247
0.04620.000380.000190.000190.462
0.00095
0.000019
0.000211
0.00760.0000821
0.00760.000493”Urinary path” in Figure 14-1
”Other kidney tissue” in Figure 14-1(864) By analogy with plutonium the liver is divided into compartments representing
hepatocytes (Liver 1) and Kupffer cells (Liver 2). The deposition fraction assigned to theliver is 0.05. Thorium depositing in the liver is assigned to Liver 1. The removal half-timefrom Liver 1 is 1 y. Half (50%) of activity leaving Liver 1 is assigned to Liver 2, 25% is
assigned to blood, and 25% is assigned to the small intestine contents (representing biliary
secretion). The long-term retention compartment, Liver 2, is assumed to lose activity toblood with a biological half-time of 9 y. In addition to endogenous faecal excretion ofthorium via liver bile, it is assumed that 0.5% of thorium leaving plasma is secreted into theright colon contents and subsequently excreted in faeces.
(865) The kidneys are assumed to consist of two compartments, one with relatively shortretention and one with relatively long retention. These compartments are referred to as theurinary path and other kidney tissue, respectively. The urinary path receives thorium from281

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
11224
11225
11226
11227
11228
11229
11230
11231
11232
11233
11234
11235
11236
11237
11238
11239
11240
11241
11242
11243
11244
11245
11246
11247
11248
11249
11250
11251
11252
11253
11254
11255
11256
11257
11258
11259
11260
11261
11262
11263
11264
11265
11266
11267
11268
11269
11270
11271

plasma and loses activity to the urinary bladder contents. Other kidney tissue receives thoriumfrom blood and loses thorium to blood. It is assumed that 3.5% of outflow from plasma
deposits in the urinary path and 1% deposits in other kidney tissue. The removal half-timefrom the urinary path to the urinary bladder contents is 15 d. The removal half-time fromother kidney tissue is 5 y. It is further assumed that 5.5% of activity leaving the circulation
moves instantaneously through the kidneys and deposits in urinary bladder contents. Hence, a
total of 9% of thorium leaving the circulation is assumed to enter urinary excretion pathways.
(866) The model describing uptake and removal of thorium by the gonads is the default
model for the actinide elements. It is assumed that deposition in the gonads, expressed as apercentage of thorium leaving the circulation, is 0.001% per gram of gonadal tissue. This
yields a deposition of 0.035% of thorium leaving the circulation in the 35-g testes of thereference adult male and 0.011% in the 11-g ovaries of the reference adult female (ICRP,
2002). The removal half-time from gonads to blood is assumed to be 10 y.
(867) Other soft tissues are divided into compartments ST0, ST1, and ST2 representing
fast, moderate, and slow return of thorium to blood. These compartments and associatedparameter values are defined on a kinetic basis and are not physically identifiable entities.
They are based mainly on observations of the time-dependent content of soft tissues otherthan liver and kidneys following intravenous administration of thorium to laboratory animals.
As described earlier, it is assumed that 30% of outflow from blood deposits in ST0. It is
assumed that 2% of activity leaving the circulation deposits in compartment ST2. The
percentage left over after all other deposition fractions in the model have been chosen,
amounting to ~12.5% of thorium leaving the circulation, is assigned to theintermediate-turnover soft-tissue compartment, ST1. The removal half-times from ST0, ST1,and ST2 are 1.5 d, 2 y, and 100 y, respectively.
14.2.3.3. Treatment of radioactive progeny(868) The dosimetrically significant progeny of thorium isotopes addressed in this report
are isotopes of actinium, thorium, protactinium, uranium, radium, radon, polonium, lead,bismuth, thallium, actinium, francium, or astatine.
(869) The characteristic model for thorium described above is applied to thorium isotopes
produced in systemic compartments by serial decay of members of a thorium chain. Thorium
produced in a compartment that is not identifiable with a compartment in the characteristic
model for thorium is assumed to transfer to the central blood compartment at the rate 1000 d-1
if produced in a blood compartment and at the rate of bone turnover if produced in an
exchangeable bone volume compartment. The model for thorium is also applied toprotactinium produced in systemic compartments following intake of a thorium parent.
(870) The characteristic model for uranium is applied to uranium produced in systemiccompartments following intake of a thorium parent. Uranium produced in a compartmentthat is not identifiable with a compartment in the characteristic model for uranium (which
occurs only for certain soft-tissue compartments) is assumed to transfer to the central bloodcompartment at the rate 0.0347 d-1 (half-time of 20 d), the rate of loss from the intermediateterm compartment of Other soft tissues in the characteristic model for uranium.
(871) The models for actinium, radium, radon, polonium, lead, bismuth, thallium,
actinium, francium, and astatine produced systemically by serial decay of members of athorium chain are essentially the same as the models applied to these elements as progeny ofradium (see the section on radium).

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11272
11273
11274
11275
11276
11277
11278
11279
11280
11281
11282
11283
11284
11285
11286
11287
11288
11289
11290
11291
11292
11293
11294

14.3.

Individual monitoring

228Th(872) 228Th monitoring techniques include urine and faeces bioassay. Care must be taken
when interpreting intakes of 228Th though measurements of the nuclide concentrations in
excreta samples due to presence of natural thorium. Th-228 itself cannot be detected directly
by in vivo measurement. The body content of Th-228 can be inferred from the measurementof the gamma emissions of the decay products, Pb-212 or Tl-208. Assumptions concerning
the equilibrium ratio between 228Th and its decay products are required. The ratios ofdaughters’ activities to Th-228 in the source material are important. Depending on theseratios monitoring done immediately after exposure might be strongly influenced by inhaled
Rn-220. The biokinetics of Pb-212 in the lung should be considered, as Pb-212 might have afaster clearing rate from the lungs than thorium.
(873) In addition, as explained in section 2.1, in the paragraphs describing Decay productsof thorium formed in the lungs, a fraction of the daughters formed within the lung will leave
the lung in a faster clearing rate, not taken into account on the bioassay functions described inthis series of documents. The underestimation due to the loss of decay products by alpharecoil should be added to the uncertainty of the result.
(874) Measurement of thoron (Rn-220) in breath is a potentially useful technique fordetermining lung burdens of Th-228. The uncertainties in the assessment of lung burdens are
difficult to quantify and may underestimate the lung burdens, as explained in section 2.1,
Emanation of radon: recoil and diffusion.
IsotopeMonitoring
Technique

228

Urine Bioassay
Faeces Bioassay
Lung Counting

Th
Th
228
Th
228

11295
11296
11297
11298

of Typical
DetectionLimit
α spectrometry
1 mBq/L
α spectrometry
2mBq/24h
γ-ray spectrometry 10 Bq (of Pbof 212 Pb
212)

Achievabledetection limit
0.1 mBq/L
0.2 mBq/24h
8 Bq (of Pb-212)229Th(875) Urine bioassay is used to determine 229 Th intakes.

IsotopeMonitoring
Technique229

Urine Bioassay

Th

11299
11300
11301
11302

MethodMeasurement

MethodMeasurementof Typical
DetectionLimit
α spectrometry
2 mBq/L

Achievabledetection limit

230Th(876) 230Th intakes are determined though urine and faeces bioassay.
IsotopeMonitoring
Technique

230

Urine Bioassay
Faeces Bioassay

Th
Th

230

MethodMeasurementof Typical
DetectionLimit
α spectrometry
1 mBq/L
α spectrometry
2 mBq/24h

11303

283

Achievabledetection limit
0.05 mBq/L
0.2 mBq/24h

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
11304
11305
11306
11307
11308
11309
11310
11311
11312
11313
11314
11315
11316
11317
11318
11319
11320
11321
11322
11323
11324
11325
11326
11327
11328
11329
11330
11331
11332
11333
11334
11335
11336
11337
11338
11339
11340

232

Th
(877) Intakes of 232Th are determined by in vitro bioassay of urine samples, complemented
or not by analysis of faeces. In general it is necessary to use the most sensitive measurement
technique to be able to detect Th-232 exposures at the investigation levels. As thorium is a
nuclide naturally present in the environment and in the diet, excretion rates of natural thorium
are expected and should be evaluated for the population in the region of residence of theworkers. This is especially important for the interpretation of faeces sample results.
(878) Th-232 itself cannot be detected directly by in vivo measurement. In vivo lungcounting is performed using the measurement of its decay products.. Assessment of Th-232
lung content by the measurement of the gamma emissions of daughter nuclides is notstraightforward. It depends on equilibrium assumptions in the source material that the worker
is exposed and on the biokinetics of the chain members in the lung. For sources of exposurein which Th-232 is presumed in equilibrium with the daughters, Ac-228 is in general chosen
to be measured, because no assumptions about Rn-220 are needed to calculate thecorresponding Th-232 activity. As explained in section 2.1, in the paragraphs describing
Decay products of thorium formed in the lungs, Ra-228 and Ac-228 have faster clearing rates
from the lungs than thorium. In addition, a fraction of the daughters formed within the lungwill leave the lung in a faster clearing rate, not taken into account on the bioassay functions
described in this series of documents. The underestimation due to the loss of decay products
by alpha recoil should be added to the uncertainty of the result.
(879) When the source of exposure is a purified thorium source, containing only Th-232
and Th-228, in equal quantities immediately after purification, Ac-228 will not be measurable
for a long time. On the other hand, in about three weeks Pb-212 will be in equilibrium with
Th-228, and may be used to assign Th-232 intakes, keeping in mind the uncertainties onunderestimation of thorium due to the faster clearing rate of the daughter products formed
within the lung. If the Th-232 source is purified again, depending on the amount of Th-228
which is left, the measurement of Pb-212 will underestimate the Th-232, and may not be
useful even for screening.
(880) Thus in order to estimate Th-232 content using lung monitoring of the daughter
products, it is necessary to know the ratios of daughters activities to Th-232 in the source of
exposure. In addition the biokinetics of daughter products in the lung should be carefully
evaluated.
(881) Measurement of thoron (Rn-220) in breath is a potentially useful technique fordetermining lung burdens of Th-232. The uncertainties in the assessment of lung burdens are
difficult to quantify and may underestimate the lung burdens, as explained in section 2.1,
Emanation of radon: recoil and diffusion.
IsotopeMonitoring
Technique232

Urine Bioassay
Urine Bioassay
Faeces Bioassay
Lung Counting

Th
Th
232
Th
232
Th
232

MethodMeasurementof Typical
DetectionLimit
α spectrometry
1 mBq/L
ICPM/S
0.3 mBq/L
α spectrometry
2 mBq/24h
γ-ray spectrometry 20 Bq of228
of 228Ac
Ac

11341
11342
11343

284

Achievabledetection limit
0.05 mBq/L
0.06 mBq/L
0.2 mBq/24h
10 Bq of 228Ac

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
11344
11345
11346
11347

234

Th
(882) 234Th is a gamma emitter. Its intake may be determined through bioassay analysis ofurine samples or though in vivo lung counting.
IsotopeMonitoring
Technique

234
234

Th
Th

11348
11349
11350
11351
11352
11353
11354
11355
11356
11357
11358
11359
11360
11361
11362
11363
11364
11365
11366
11367
11368
11369
11370
11371
11372
11373
11374
11375
11376
11377
11378
11379
11380
11381
11382
11383
11384
11385
11386
11387
11388
11389

MethodMeasurement

Achievabledetection limit

Urine Bioassay

of Typical
DetectionLimit
γ-ray spectrometry
4 Bq/L

Lung Counting

γ-ray spectrometry

30 Bq

50 Bq

0.09 mBq/L

References
Albert, R.E., 1966. Thorium: Its Industrial Hygiene Aspects. Academic Press, New York.
Ballou, J.E., Hursh, J.B., 1972. The measurement of thoron in the breath of dogs administeredinhaled or injected ThO2. Health Phys., 22, 155–159.
Ballou, J.E., Gies, R.A., Case, A.C., Haggard, D.L., Bushbom, R.L., Ryan, J.L., 1986. Deposition andearly disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat. Health Phys. 51
755-771.
Bečková, V., Malátová, I., 2008. Dissolution behaviour of 238U, 234U and 230Th deposited on filtersfrom personal dosemeters. Radiat. Prot. Dosim. 129(4): 469-472, published ahead of print
November 1, 2007 doi:10.1093/rpd/ncm455.
Boecker, B.B., 1963. Thorium distribution and excretion studies III. Single inhalation exposure to
the citrate complex and multiple inhalation exposures to the chloride. Am. Ind. Hyg. Assoc.
J. 24, 155–163.
Boecker, B.B., Thomas, R.G., Scott, J.K., 1963. Thorium distribution and excretion studies II.
General patterns following inhalation and the effect of the size of the inhaled dose. HealthPhys. 9, 165–176.
Chen Xing-an, Xiao Hui-juan, Cheng Yong-e, Yang Ying-je, 1995. An observation on the clearanceof thorium dioxide from the lung of a miner. J. Radiol. Prot. 15, 343–346.
Chen Xing-an, Xiao Hui-juan, Dong Zhihua, Lu Hiu Min, Yang Yingjie, Wang Ji Zhong, Wang
Yidien, Li Shou-Hua, Hu Ya Qin, 1988. An assessment of the estimated thorium lungburdens of 130 miners in a rare-earth and iron mine in China. In Inhaled Particles VI,
Proceedings of an International Symposium and Workshop on Lung Dosimetry Organisedby the British Occupational Hygiene Society in Co-operation with the Commission of theEuropean Communities, Cambridge, 2-6 September 1985, (Eds. Dodgson, J., McCallum,
R.I., Bailey, M.R., and Fisher, D.R), Pergamon Press, Oxford, United Kingdom. Ann.
Occup. Hyg., 32 (Suppl. 1), 871 – 876.
Coombs, M.A., Cuddihy, R.G., 1983. Emanation of 232U daughter products from submicron particles
of uranium dioxide and thorium dioxide by nuclear recoil and inert gas diffusion. J Aerosol
Sci. 14, 75-86.
Dang, H.S., Jaiswal, D.D., Murthy, K.B., Sharma, R.C., Nambiar, P.P., Sunta, C.M., 1992. Relevanceof ICRP metabolic model of thorium in bio-assay monitoring. J. Radioanalytical Nucl.
Chem. Articles 156, 55-64.
Duport, P., Edwardson, E., 1984. Characterization of radioactive long-lived dust present in uranium
mines and mills atmospheres. In: Stocker, H. (Ed.), Proc. Int. Conf. on occupationalradiation safety in mining, pp. 189–195. Toronto, Canadian Nuclear Association.
Duport, P., Robertson R., Ho K., Horvath F., 1991. Flow-through dissolution of uranium-thorium ore
dust, uranium concentrate, uranium dioxide, and thorium alloy in simulated lung fluid.
Radiat. Prot. Dosim. 38(1/3), 121-133.
Fisher, D.R. Jackson, P.O., Brodaczynski, G.G., Scherpelz, R.I., 1983. Levels of 238U and 230Th in
excreta of uranium mill crushermen. Health Phys. 45, 617-629.

285

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
11390
11391
11392
11393
11394
11395
11396
11397
11398
11399
11400
11401
11402
11403
11404
11405
11406
11407
11408
11409
11410
11411
11412
11413
11414
11415
11416
11417
11418
11419
11420
11421
11422
11423
11424
11425
11426
11427
11428
11429
11430
11431
11432
11433
11434
11435
11436
11437
11438
11439
11440
11441

Glover, S.E., Traub, R.J., Grimm, C.A., Filby, R.H., 2001. Distribution of natural thorium in thetissues of a whole body. Radiat. Prot. Dosim. 97, 153-160.
Gray, S.A., Stradling G.N., Moody J.C., Pearce, M.J., Hodgson, A., Ellender, M., 1991. Biokineticsof Thorium in the Rat after Administration as Nitrate: Implications for Human Exposure.
NRPB-M281, Chilton, Didcot, Oxon OX11 0RQ.
Griffiths W.C., Cuddihy, R.G., Hoover, M.D. Stalnaker, N.D. 1980. Simulation of the retention anddosimetry of 232U and its daughters after inhalation in ThO2 or UO2 particles. In: Sanders C.
L., Cross F.T., Dagle G. E., Mahaffey, J.A., (Eds.), Pulmonary Toxicology of Respirable
Particles. pp. 193-208. Proc. 19th Annual Hanford Life Sciences Symposium at Richland,
WA, October 22-24, 1979. CONF-791002. Available from National Technical Information
Service. Springfield. Virginia.
Hamilton, E.I., Minsky, M.J., Cleary, J.J., 1972. The concentration and distribution of some stableelements in healthy human tissues from the United Kingdom. Sci. Total Environ., 1, 341374.
Hodge, H.C., Thomas, R.G., 1959. The questions of health hazards from the inhalation of insolubleuranium and thorium oxides. In: Marley, W.G., Morgan, K.Z. (Eds.), Progress in Nuclear
Energy, Series XII, Health Physics. Pergamon Press pp. 52 – 59.
Hodgson, S.A., Rance, E.R., Stradling, G.N., Hodgson, A., Fell, T.P., Youngman, M.J., Moody, J.C.,
Ansoborlo, E., 2000. Biokinetics of thorium dioxide and its decay products in the rat after
alveolar deposition: implications for human exposure. Chilton, NRPB-M1192.
Hodgson, S.A., Stradling, G.N., Hodgson, A., Smith, T.J., Youngman, M.J., Moody, J.C., Ansoborlo, E.
2003. Biokinetics and assessment of intake of thorium dioxide. Radiat. Prot. Dosim. 105,
115–118.
Ibrahim, S.A., Wrenn, M.E., Singh, N.P., Cohen, N., Saccomanno, G., 1983. Thorium concentrationin human tissues from two U. S. populations. Health Phys. 44, Suppl. 1, 213-220.
ICRP, 1979. International Commission on Radiological Protection. Limits on Intakes ofRadionuclides for Workers. ICRP Publication 30, Pt.1. Pergamon Press, Oxford. Ann. ICRP
2, (3/4).
ICRP, 1993. International Commission on Radiological Protection. Age-dependent Doses toMembers of the Public from Intake of Radionuclides. Pt.2. ICRP Publication 67. Pergamon
Press, Oxford. Ann. ICRP. 23, (3/4).
ICRP, 1994a. Dose Coefficients for Intakes of Radionuclides by Workers, ICRP Publication 68. Ann.
ICRP 24(4). Oxford, Pergamon Press.
ICRP, 1994b. International Commission on Radiological Protection. Human respiratory tract model
for radiological protection. ICRP Publication 66, Ann. ICRP 24 (1-3).
ICRP, 1995a. Age dependent Doses to Members of the Public from Intakes of Radionuclides: Part 3.
Ingestion dose coefficients. ICRP Publication 69. Ann. ICRP 25(1). Oxford, Pergamon
Press.
ICRP, 1995b. Age-dependent Doses to Members of the Public from Intake of Radionuclides. Pt.4:
Inhalation Dose Coefficients. ICRP Publication 71. Pergamon Press, Oxford. Ann. ICRP.
25, (3 - 4).
ICRP, 2002. Basic anatomical and physiological data for use in radiological protection: Reference
values, ICRP Publication 89, Ann. ICRP 32(3/4). International Commission on RadiologicalProtection. Oxford, Pergamon Press.
Jaiswal, D.D., Singh, I.S., Nair, S., Dang, H.S., Garg, S.P., Pradham, A.S., 2004. Comparison ofobserved lung retention and urinary excretion of thorium workers and members of the
public in India with the values predicted by the ICRP biokinetic model. Radiat. Prot. Dosim.
112, 237-243.
Johnson, J.R., Peterman, B.F. 1984. A model to describe thoron exhalation following an inhalation
exposure to thoria aerosols. In: Smith, H., Gerber, G. (Eds.) Lung Modelling for Inhalation ofRadioactive Materials. EUR 9384. pp. 193 – 197 Commission of the European Communities,
Luxemburg.

286

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
11442
11443
11444
11445
11446
11447
11448
11449
11450
11451
11452
11453
11454
11455
11456
11457
11458
11459
11460
11461
11462
11463
11464
11465
11466
11467
11468
11469
11470
11471
11472
11473
11474
11475
11476
11477
11478
11479
11480
11481
11482
11483
11484
11485
11486
11487
11488
11489
11490
11491
11492

Johnson, J.R., Lamothe, E.S., 1989. A Review of the Dietary Uptake of Th. Health Phys. 56, 165168.
Kalkwarf, D.R., Jackson, P.O., Kuti, J.C., 1985. Emanation coefficients for Rn in sized coal fly ash.
Health Phys. 48, 429–436.
LaMont, S.P., Filby, R.H., Glover, S.E., 2001. In vitro dissolution characteristics of aged andrecrystallised high-fired 232ThO2. Radiat. Prot. Dosim, 14, 75-86.
Larsen, R.P., Oldham, R.D., Bhattacharyya, M.H., Moretti, E.S., 1984. Gastrointestinal absorption
and distribution of thorium in the mouse. In: Environmental Research Division annual
report, July 1982-June 1983; Argonne National Laboratory, ANL-83-100-Pt. 2; pp. 65-68.
Leggett, R.W., 1997. Basis and implications of the ICRP’s new biokinetic model for thorium. HealthPhys. 73, 587-600.
Lipsztein, J.L., Bertelli, L.N., Oliveira, C.A.N., Azeredo, A.M.G., Melo, D.R., Lourenco, M.C.,
Grynspan, D., Dantas, B.M., 1989. Bioassay monitoring studies for thorium. Radiat. Prot.
Dosim. 26, 57-60.
Maletskos, C.J., Keane, A.T., Telles, N.C., Evans, R.D., 1966. The metabolism of intravenously
administered radium and thorium in human beings and the relative absorption from thehuman gastrointestinal tract of radium and thorium in simulated radium dial paints. In:
Radium and mesothorium poisoning and dosimetry and instrumentation techniques inapplied radioactivity (MIT-952-3), Massachusetts Institute of Technology, Cambridge,
Massachusetts; pp. 202-317.
Maletskos, C.J., Keane, A.T., Telles, N.C., Evans, R.D., 1969. Retention and absorption of 224Ra and234
Th and some dosimetric considerations of 224Ra in human beings. In: (Mays, C.W., Jee,
W.S.S., Lloyd, R.D., Stover, B.J., Dougherty, J.H., Taylor, T.N. (Eds.), Delayed Effects ofBone-seeking Radionuclides University of Utah Press, Salt Lake City. pp. 29-49.
Maniyan, C.G., Pillai, P.M., Khan, A.H., 2000. An in vivo study on clearance of thorium from thethorax. Radiat.Prot.Dosim. 90(4), 423-427.
Marsh J.W., Gregoratto, D., Karcher, K., Nosske D., Bessa Y., Blanchardon E., Hofmann W.,
Tomasek L., 2011. Dosimetric calculations for uranium miners for epidemiological studies.
Radiat Prot Dos pp. 1-13, doi:10.1093/rpd/ncr310..
Mausner, L.F., 1982. Inhalation exposures at a thorium refinery. Health Phys. 42, 231–236.
Moody, J.C., Davies, C.P., Stradling, G.N., 1994b. Biokinetics of thorium and daughter radionuclides
after deposition in the rat lung as fluoride and hydroxide. In: Mohr, U., Dungworth, D.L.,
Mauderly, J.L., Oberdörster, G. (Eds.), Proc. Fourth International Inhalation Symposium,
Hannover, March 1-5, 1993. Toxic and Carcinogenic Effects of Solid Particles in the
Respiratory System, pp. 611-614.
Moody, J.C., Stradling, G.N., Pearce, M.J., Gray, S.A., 1994a. Biokinetics of thorium and daughter
radionuclides after deposition in the rat lung as nitrate: implications for human exposure.
NRPB–M525, Chilton, UK.
Moody, J.C., Stradling, G.N., 1992. Biokinetics of thorium and daughter radionuclides after
deposition in the rat lung. J. Aerosol Sci. 23, Suppl. 1, S523–S526.
Newton, D., Rundo, J., Eakins, J.D., 1981. Long term retention of 228Th following accidental intake.
Health Phys. 40, 291–298.
Pavlovskaya, N.A., Provotorov, A.V., Makeeva, L.G., 1971. Absorption of thorium from thegastrointestinal tract into blood of rats and build-up in organs and tissues. Gig. Sanit. 36,
47-50.
Reif, R.H., 1994. Evaluation of in vitro dissolution rates of thorium in uranium mill tailings. HealthPhys., 67, 545-547.
Roth, P., Höllriegl, V., Li, W.B., Oeh, U., Schramel, P., 2005. Validating an important aspect of the
new ICRP biokinetic model of thorium. Health Phys 88, 223-228.
Rundo, J., 1964. Two cases of chronic occupational exposure to radioactive materials. In: Assessmentof radioactivity in man, Vol. II (Vienna: IAEA); pp. 291-306.

287

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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11494
11495
11496
11497
11498
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11501
11502
11503
11504
11505
11506
11507
11508
11509
11510
11511
11512
11513
11514
11515
11516
11517
11518
11519
11520
11521
11522
11523
11524
11525
11526
11527
11528
11529
11530
11531
11532
11533
11534
11535
11536
11537
11538
11539
11540
11541
11542
11543

Rundo, J., Brewster, D.R., Essling, M.A., Sha, J.Y., 1981. Radioactivity in former workers at athorium refinery. In: Wrenn, M.E. (Ed.), Actinides in Man and Animals, Proceedings of the
Snowbird Actinide Workshop, pp. 261–267. Radiobiology Division, University of Utah,
Salt Lake City, RD Press.
Rundo, J., Toohey, R.E., 1986. Long-term retention of thorium in lung: Report of a case. HealthPhys., 50, Suppl. 1, S24.
Scott, J.K., Neuman, W.F., Bonner, J.F., 1952. The distribution and excretion of thorium sulphate. J.
Pharmacol. Exp. Ther. 106, 286–290.
Singh, N.P., Wrenn, M.E., Ibrahim, S.A., 1983. Plutonium concentration in human tissues:Comparison to thorium. Health Phys. 44, Suppl. 1, 469-476.
Singh, N.P., Zimmerman, C.J., Taylor, G.N., Wrenn, M.E., 1988. The beagle: An appropriate
experimental animal for extrapolating the organ distribution pattern of thorium in humans.
Health Phys. 54, 293-299.
Singh, N.P., Bennett, D.D., Wrenn, M.E., 1987. Concentrations of α-emitting isotopes of U and Th
in uranium miners' and millers' tissues. Health Phys., 53, 261–265.
Stebbings J.H., 1985. Personal factors affecting thoron exhalation from occupationally acquired
thorium body burdens. Environmental Research Division, Center for Human Radiobiology,
Annual Report June 1983 – June 1984, ANL-84-103 Part II, pp. 60 – 74. Argonne National
Laboratory.
Stehney, A.F., Lucas, H.F., 2000. Thorium isotopes in autopsy samples from thorium workers. HealthPhys. 78, 8-14.
Stehney, A.F., Polednak, A.P., Rundo, J., Brues, A.M., Lucas, H.F., Patten, B.C., Rowland, R.E.,
1980, Health status and body radioactivity of former thorium workers. Argonne National
Laboratory; NUREG/CR-1420 ANL-80-37.
Stover, B.J., Atherton, D.R., Keller, N., Buster, D.S., 1960. Metabolism of the Th-228 decay series inadult beagle dogs. Radiat. Res. 12, 657-671.
Stradling, G.N., Hodgson, A., Fell, T.P., Phipps, A.W., Etherington, G., 2004. Thorium Nitrate andDioxide: Exposure Limits and Assessment of Intake and Dose after Inhalation NRPB–W57,
Chilton, UK. Available at www.hpa.org.uk
Stradling, G.N., Davies, C.P., Moody, J.C., Gray, S.A., Wilson, I., Ellender, M., 2005b. Biokineticsof thorium and daughter radionuclides after deposition as fluoride and hydroxide in the rat
lung: implications for occupational exposure. NRPB-DA/05/2005, Chilton, UK.
Stradling, G.N., Gray, S.A., Moody, J.C., Ellender, M., Pearce, M.J., 2005a. Biokinetics of thorium inthe presence of a highly transportable form of uranium: implications for occupational
exposure. NRPB-DA/04/2005, Chilton, UK.
Strong, K.P., Levins, D.M., 1982. Effect of moisture content on radon emanation from uranium ore
and tailings. Health Phys. 42, 27–32.
Stuart, B.O., Jackson, P.O., 1975. The inhalation of uranium ores. In: Proceedings of the Conferenceon Occupational Health Experience with Uranium. Arlington, Virginia, April 28–30, 1975,
ERDA 93 (Ed. Wrenn, M.E.). US Energy Research and Development Administration, pp.
130–139. Available from National Technical Information Service, Springfield, Virginia.
Stuart, B.O. Beasley, T.M., 1967, Non-equilibrium tissue distributions of uranium and thorium
following inhalation of uranium ore by rats. In: Davies, C.N., (Ed.), Inhaled Particles andVapours II. Proceedings of an International Symposium organised by the British
Occupational Hygiene Society; Cambridge, UK. Oxford: Pergamon Press pp. 291-8.
Sullivan, M.F., 1980. Absorption of Actinide Elements from the Gastrointestinal tract of rats, guinea
pigs, pigs and dogs. Health Phys. 38, 159-171.
Sullivan, M.F., Miller, B.M., Ryan, J.L., 1983. Absorption of thorium and protactinium from thegastrointestinal tract in adult mice and rats and neonatal rats. Health Phys. 44, 425-428.
Sunta, C.M., Dang, H.S., Jaiswal, D.D., 1987. Thorium in man and environment, uptake andclearance. J. Radioanal. Nucl. Chem., 115, 149-158.

288

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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11545
11546
11547
11548
11549
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11551
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11554
11555
11556
11557
11558
11559
11560
11561
11562
11563
11564
11565

Terry, K.W., Hewson, G.S., 1995. Thorium lung burdens of mineral sands workers. Health Phys. 69,
233–242.
Terry, K.W.,, Hewson, G.S., 1993. Retention and excretion of thorium by mineral sands industry
employees. Minerals and Energy Research Institute of Western Australia; Report No. 117.
Thomas, R.G., Lie, R., Scott, J.K., 1963. Thorium distribution and excretion studies I. Patterns
following parenteral administration. Health Phys. 9, 153–163.
Toohey R.E., Rundo, J., Sha J.Y., Essling M.A., Pedersen J.C., Slane J.M. 1985. Activity ratios ofthorium daughters in vivo. Environmental Research Division, Center for HumanRadiobiology, Annual Report June 1983 – June 1984, ANL-84-103 Part II, pp. 53 – 59.
Argonne National Laboratory.
Traikovich, M., 1970. Absorption, distribution and excretion of certain soluble compounds of natural
thorium. In: Letavet, A.A., Kurlyandskaya, E.B. (Eds.), Toxicology of radioactive
substances, Vol. 4: thorium-232 and uranium-238. English Translation (G.W. Dolphin, Ed.).
Pergamon Press, Oxford.
Wrenn, M.E., Singh, N.P., Cohen, N., Ibrahim, S.A., Saccomanno, G., 1981. Thorium in humantissues. NUREG/CR–1277, US Nuclear Regulatory Commission. Available from National
Technical Information Service, Springfield, Virginia.
Wrenn, M.E., Singh, N.P., Paschoa, A.S., Lloyd, R.D., and Saccomanno, G. (1985). Concentration of
U and Th Isotopes in U Miners' and Millers' Tissues. NUREG/CR 4382, U.S. Nuclear
Regulatory Commission, Washington, D.C. Available from National Technical Information
Service, Springfield, Virginia.

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15.
15.1.

Chemical forms in the workplace(883) Uranium is an actinide element which mainly occurs in oxidation states IV and VI. It
is encountered in industry in a variety of chemical and physical forms, including oxides (UO3,
UO4, UO2, U3O8, uranates), inorganic salts (nitrates, chlorides, fluorides, carbonates,
phosphates) and some organic compounds (acetylacetonate, Tri-Butyl-Phosphate). Someforms, notably the metal, carbide and oxide may be encountered as depleted uranium (~ 0.2%
235U), natural (0.7% 235U) or enriched (>0.7% 235U) uranium. The chemical behavior of any
given uranium compound will be similar irrespective of whether it is present in natural,
depleted or enriched form. Depleted uranium has found use as a shielding material inaeronautics and military applications such as counterweights for aircraft control surfaces.
238
U, 235U, and 234U, are the three major isotopes and 235U is typically the main fissile material
for nuclear power reactors. It should be noted that intakes of the more readily absorbed
uranium compounds are limited by considerations of chemical toxicity rather than radiationdose (ICRP, 1997).
Table 15-1. Isotopes of uranium addressed in this report
Isotope
U-230
U-231
U-232
U-233
U-234aU-235aU-235m
U-236
U-237
U-238a
U-239
U-240
U-242

11587
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11600

URANIUM (Z = 92)

a

15.2.

Physical half-life
20.8 d4.2 d68.9 y1.592E+5 y
2.455E+5 y
7.04E+8 y
26 m
2.342E+7 y
6.75 d
4.468E+9 y
23.45 m14.1 h
16.8 mDecay mode
A
EC, A
A
A
A
A
IT
A
BA,SF
BBB-

Data for these radionuclides are given in the printed copy of this report. Data for otherradionuclides are given on accompanying electronic disk.

Routes of Intake

15.2.1. Inhalation(884) There is extensive information available on the behaviour of uranium after
deposition in the respiratory tract from animal experiments (mainly in rats), in vitro
dissolution studies, and some accidental human intakes. Much of this information has beenobtained since the issue of Publication 30 (ICRP, 1979). Absorption parameter values havebeen derived from the results of animal and in vitro studies for a wide range of compounds
encountered in the nuclear fuel industry. Ansoborlo et al. (2002) and Stradling et al. (2002)
compiled absorption parameter values derived from the results of a large number of in vivo

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11641
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11646
11647
11648

and in vitro studies carried out on materials from French and UK nuclear fuel fabrication
facilities.
(885) Absorption parameter values and Types, and associated fA values for particulate
forms of uranium are given in Table 15-2.
Absorption parameter values and Types
Uranium hexafluoride (UF6)(886) Uranium hexafluoride exists in vapour form, but in the presence of water in theatmosphere and in the respiratory tract it is converted to uranyl fluoride (UO2F2) aerosol.
Generally, any exposure would be to both chemical forms simultaneously, and also to HF
fumes. Hence, the mixture is treated here as an aerosol rather than a vapour. In experimentswith beagle dogs (Morrow et al., 1982), 80% of the initial lung deposit (ILD) of uranium wasabsorbed into blood within 20 minutes. The rapid urinary excretion observed after accidental
inhalation exposures by humans (Boback, 1975, Beau and Chalabreysse, 1989, Fisher et al.,1991) indicates assignment to default Type F. The rapid absorption half-time was estimatedby the task group to be 45 minutes (sr = 22 d-1) from the data of Fisher et al. (1991).
Absorption parameter values derived here from urinary excretion data presented by Beau andChalabreysse (1989) are fr = 1 and sr = 1.6 d–1. Bailey and Davis (2002) derived absorption
parameter values of fr = 1 and sr = 1.5 d–1 from daily urinary excretion data presented by
Moore and Kathren (1985) for an accidental intake by a worker (Case G) described by
Boback (1975). However, the detailed data for the first two days after exposure reported by
Boback (1975) show faster absorption (sr ~100 d–1) of much of the uranium. In view of thewide range of values of sr derived from the studies above, these data are judged to be an
insufficient basis to provide specific absorption parameter values and UF6 is therefore
assigned to Type F.
Uranyl Tri-Butyl-Phosphate (U-TBP)(887) Tri-n-Butyl-Phosphate (TBP) is used extensively as an extractant during fabricationof nuclear fuel and for the separation of uranium and plutonium during reprocessing. Afteradministration of U-TBP to rats by intratracheal instillation, 80–90% of the U was absorbed
into blood by about 1 d after exposure (Pellow et al., 1996; 1997). Absorption parametervalues derived from the results by Stradling et al. (2002) were fr = 0.97, sr = 12 d–1 and ss =0.0021 d–1. From results of a complementary gavage experiment it was estimated thatfractional absorption from the alimentary tract fA = 0.022.
(888) Specific absorption parameter values of fr = 0.97, sr = 12 d–1 and ss = 0.002 d–1(consistent with assignment to default Type F) and fA = 0.02 are used here for U-TBP.
Uranyl nitrate (UO2(NO3)2)(889) Uranyl nitrate in aqueous solution is widely encountered in nuclear fuel fabrication
and reprocessing. Ballou et al. (1986) followed the biokinetics of 232U and 233U in rats for 200
days after inhalation of aerosols of aqueous uranyl nitrate solution: 15–45% ILD was retainedin the lung at 30 d, depending on particle size, supporting assignment to default Type M.
Measurements made after intratracheal instillation into rat lungs are consistent withassignment to default Type F (Cooper et al., 1982, Ellender, 1987, Stradling et al., 2005).
Ballou et al. (1986) reported that 1 hour after instillation of 232U or 233U nitrate, only 22%
ILD remained in the lungs, with systemic uptake of at least 40% ILD. Hodgson et al. (2000)
derived absorption parameter values of fr = 0.93, sr = 3 d-1 and ss = 0.005 d–1 from the results
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11666
11667
11668
11669
11670
11671
11672
11673
11674
11675
11676
11677
11678
11679
11680
11681
11682
11683
11684
11685
11686
11687
11688
11689
11690
11691
11692
11693
11694
11695
11696

of the study by Ellender (1987) in which the biokinetics of uranium were followed for 30days after intratracheal instillation of uranyl nitrate. The available human and animal data
indicate that a value of 0.02 for fractional absorption in the alimentary tract is appropriate foroccupational exposures to UO2(NO3)2.6H2O.
(890) Specific absorption parameter values of fr = 0.9, sr = 3 d-1 and ss = 0.005 d–1(consistent with assignment to default Type F) and fA = 0.02 are used here for uranyl nitrate.
Ammonium diuranate (ADU) (NH4)2U2O7(891) ADU is a basic product in the uranium fuel cycle, a component of “yellow cake” (ageneric term for material which may comprise ADU, U3O8 or a mixture of both). Stradling etal. (1987) followed the biokinetics of uranium for 360 days after inhalation of ADU by rats.
At 7 days, 11% ILD remained in the lung and 70% ILD was absorbed into blood. From theseresults, Hodgson et al. (2000) derived parameter values of fr = 0.85 and sr = 0.78 d-1: the valueof ss was too low to be determined and was taken to be 0.005 d-1. Ansoborlo et al. (2002)
derived parameter values of fr = 0.71, sr = 0.61 d–1 and ss = 0.019 d–1 from the results of astudy in which the biokinetics of uranium were followed for 30 days after intratracheal
instillation of ADU into rats.
(892) Specific absorption parameter values of fr = 0.8, sr = 0.7 d–1 and ss = 0.02 d–1(consistent with assignment to default Type F) are used here for ADU.
Uranium peroxide hydrate (UO4.nH2O)(893) Uranium peroxide hydrate is present at one stage of the enriched uranium fuel cycle.
This compound, also expressed as UO3.H2O2.H2O, is very similar to uranium trioxide
UO3.nH2O. The dissolution and biokinetic behaviour of both compounds are very sensitive tothe hydration state (n can vary between 0 and 2.5). One main characteristic of UO4.nH2O isthat it consists of small needles with an average AMAD of about 1.1 µm. Assessments of thephysico-chemical and biokinetic properties of UO4, both in vitro and in vivo, have been
carried out (Ansoborlo et al., 1998a). The biokinetics of uranium were followed for 90 days
after intratracheal administration to rats. By 7 d after exposure 3–10% of uranium remained in
the lungs, whereas about 65% was absorbed into blood. The calculated absorption parametervalues were: fr = 0.87, sr = 0.93 d–1 and ss = 0.024 d–1 (Ansoborlo et al., 1998a). Experimental
data on ingestion of UO4 by laboratory animals, reviewed by Leggett and Harrison (1995),
suggest that absorption in the alimentary tract is about 0.5 times that of uranyl nitrate, which
is taken here to be 0.02 (see above).
(894) Specific absorption parameter values of fr = 0.9, sr = 0.9 d–1 and ss = 0.02 d–1(consistent with assignment to default Type F) and fA = 0.01 are used here for uranium
peroxide hydrate.
Uranium trioxide (UO3.nH2O)(895) In the fuel fabrication cycle, uranium trioxide is formed by heating uranyl nitrate andis then reduced to form UO2. The biokinetic behaviour of UO3.nH2O is very sensitive to thehydration state and its solubility depends on the value of n.
(896) Harris (1961) measured excretion of uranium following repeated inhalation of UO3
by a volunteer. There was considerable clearance to urine and faeces over the first few days
after each intake, indicating rapid absortion from the lower, but not from the upper,
respiratory tract. The reported measurements are not straightforward to interpret, but areasonable fit to the excretion data in the two days following the first intake was obtained
here with fr = 0.5 and sr = 0.15 d–1. Morrow et al. (1972) followed the biokinetics of uranium
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11698
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11702
11703
11704
11705
11706
11707
11708
11709
11710
11711
11712
11713
11714
11715
11716
11717
11718
11719
11720
11721
11722
11723
11724
11725
11726
11727
11728
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11731
11732
11733
11734
11735
11736
11737
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11740
11741
11742
11743
11744

for 218 days after inhalation of UO3 by dogs. Clearance from the airways was mainly to
faeces in the first day, while subsequent lung clearance was rapid, with predominantly urinary
excretion. Parameter values derived here from lung retention were: fr = 0.82, sr = 0.15 d–1 andss = 0.019 d–1 (consistent with assignment to default Type F).
(897) Hodgson et al. (2000) derived absorption parameter values from the results of astudy by Stradling et al. (1985b) in which the biokinetics of uranium were followed for 168
days after inhalation of UO3 by rats: fr = 0.92, sr = 1.4 d–1, ss = 0.0036 d–1 (consistent withassignment to default Type F). Ansoborlo et al. (2002) derived absorption parameter values
from the results of a study in which the biokinetics of uranium were followed for 30 days
after intratracheal instillation of UO3 into rats: fr = 0.71, sr = 0.28 d–1 and ss = 0.0011 d–1(consistent with assignment to default Type M). ICRP (2002), as a worked example, derived
absorption parameter values from the results of a study by Moody et al. (1997) in which the
biokinetics of uranium were followed for 42 days after intratracheal instillation of UO3 into
rats: fr = 0.77, sr = 9.2 d–1, ss = 0.0017 d–1 (consistent with assignment to default Type M).
Experimental data on ingestion of UO3 by laboratory animals, reviewed by Leggett andHarrison (1995), suggest that absorption in the alimentary tract is about 0.5 times that of
uranyl nitrate, which is taken here to be 0.02 (see above).
(898) Specific absorption parameter values of fr = 0.8, sr = 1 d–1 and ss = 0.01 d–1(consistent with assignment to default Type M) and fA = 0.01 are used here for UO3.
Uranium tetrafluoride (UF4)(899) Uranium tetrafluoride is an intermediate product in the uranium fuel cycle. It can be
reduced to uranium metal or oxidized by fluorine to form UF6. The reported biokinetic
behaviour of UF4 is complex. Measurement of urinary excretion after inhalation by workers(Chalabreysse et al., 1989) and experiments in rats and baboons (Stradling et al., 1985a,
André et al., 1989, Ansoborlo et al., 1990) showed that a large fraction (35–40%) of the lungdeposit was absorbed to the blood by 7 d after administration. However, considerable
variations in behaviour were observed, with some experiments indicating assignment todefault Type F and others to default Type M.
(900) Zhao and Zhao (1990) reported measurements of urinary excretion of uranium madefor three years after an accidental inhalation of UF4 powder by a worker. The excretion rate,
initially very low, increased to a peak at about 2 months, and then declined. To represent thisbehaviour, the alternative HRTM representation of dissolution was applied here, in whichmaterial is deposited in a compartment representing “Particles in initial state”, in which it
dissolves at a rate sp, and is simultaneously transferred at a rate spt to a compartment
representing “Particles in transformed state”, in which material dissolves at a rate st. Material
specific parameter values were derived here: sp = 0.000002 d–1; spt = 0.02 d–1; st = 0.04 d–1;
with fA = 0.0002. However, it was not possible to fit a peak as sharp as that observed. The
unusual behaviour may have been caused in part by the size of the intake, which was
sufficient to give rise to biochemical indications of kidney dysfunction.
(901) Hodgson et al. (2000) derived absorption parameter values from the results of astudy by Stradling et al. (1985a) in which the biokinetics of uranium in rats were followed for360 days after inhalation and 168 days after intratracheal administration of two forms of UF4:(i) fr = 0.51, sr = 0.10 d–1, ss = 0.0074 d–1; (ii) fr = 0.52, sr = 0.11 d–1, ss = 0.0039 d–1. Chazel etal, (2000a) derived parameter values of fr = 0.58, sr = 0.21 d–1 and ss = 0.026 d–1 from theresults of a study in which the biokinetics of uranium were followed for 30 days after
intratracheal instillation of UF4 into rats. Experimental data on ingestion of UF4 by laboratory
animals, reviewed by Leggett and Harrison (1995), suggest that absorption in the alimentary293

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11753
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11759
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11761
11762
11763
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11767
11768
11769
11770
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11772
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11779
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11781
11782
11783
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11791
11792

tract is about 0.003-0.02 times that of uranyl nitrate, which is taken here to be 0.02 (seeabove). A central value of 0.01 times that of uranyl nitrate is applied here.
(902) Specific absorption parameter values of fr = 0.6, sr = 0.15 d–1 and ss = 0.005 d–1(consistent with assignment to default Type M) and fA = 0.0002 are used here for UF4.
Uranyl acetylacetonate(903) Uranyl acetylacetonate is an organic complex of uranium with military applications.
In vitro dissolution tests in simulated lung fluid led to the classification of 50% Class D and
50% Class W (Fisher and Briant, 1994). Absorption parameter values calculated here are fr =0.52, sr = 2.5 d–1 and ss = 0.026 d–1, corresponding to default Type M. These data (in vitroonly) are judged to be an insufficient basis to propose specific absorption parameter values
and uranyl acetylacetonate is therefore assigned to Type M.
Uranium aluminide(904) As part of an epidemiological study, Leggett et al. (2005) estimated doses forworkers exposed to airborne uranium aluminide (UAlx) during the fabrication of reactor fuelplates. Occupational monitoring data included air concentrations, urine, fecal and lungmeasurements with observation periods exceeding two years in several cases. In workers who
were removed from exposure, the rate of urinary excretion of uranium increased for a few
months, peaked, and then declined at a rate consistent with moderately soluble uranium. To
represent this behaviour, the authors applied the alternative HRTM representation ofdissolution, in which material is deposited in a compartment representing “Particles in initialstate”, in which it dissolves at a rate sp, and is simultaneously transferred at a rate spt to acompartment representing “Particles in transformed state”, in which material dissolves at a
rate st. They derived material specific parameter values: sp = 0.0001 d–1, spt = 0.004 d–1, st =0.004 d–1, with fA taken to be 0.002. These parameter values are adopted here for uranium
aluminide.
Uranium octoxide (U3O8)(905) Uranium octoxide can be present in the ore concentrate (“yellow cake”, see ADU
above) and also occurs at later stages in the uranium fuel cycle. Human data from accidental
intakes of U3O8 (Saxby et al., 1964, West et al., 1979, Eidson, 1990), and from monitoringdata for workers in processing facilities (Barber and Forrest, 1995, Chalabreysse et al., 1989),
animal studies using rats, dogs and monkeys (Métivier et al., 1992, Stradling et al., 1989), andin vitro studies (Eidson, 1994, Ansoborlo et al., 1998a, Chazel et al., 1998) have shown thatthe biokinetic behaviour of this compound depends on the particular process of manufacture.
A study of the influence of specific surface area (SSA) (Chazel et al., 1998) demonstrated theimportance of this parameter on dissolution characteristics. When the SSA increased from 0.7
to 16 m2 g–1, the rapidly dissolved fraction, fr, increased from 0.01 to 0.20. At 30 d after
intake by rats and baboons, lung retention and total urinary excretion were 50-90% and 2–
10%, respectively, of the initial lung deposit.
(906) Ansoborlo et al. (2002) derived absorption parameter values from the results ofstudies in which the biokinetics of uranium were followed for 90 days after intratracheal
instillation into rats of two forms of U3O8: (i) fr = 0.046, sr = 2.25 d–1 and ss = 0.0012 d–1; (ii)fr = 0.03, sr = 2.07 d–1 and ss = 0.00038 d–1. Hodgson et al. (2000) derived absorption
parameter values from the results of a study by Stradling et al. (1987) in which the biokinetics
of uranium were followed for 360 days after inhalation by rats of uranium ore concentrate(95% U3O8, 5% UO2); fr = 0.044, sr = 0.49 d–1 and ss = 0.00035 d–1. Experimental data on
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11800
11801
11802
11803
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11805
11806
11807
11808
11809
11810
11811
11812
11813
11814
11815
11816
11817
11818
11819
11820
11821
11822
11823
11824
11825
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11827
11828
11829
11830
11831
11832
11833
11834
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11836
11837
11838
11839
11840

ingestion of U3O8 by laboratory animals, reviewed by Leggett and Harrison (1995), suggestthat absorption in the alimentary tract is about 0.01 times that of uranyl nitrate, which is taken
here to be 0.02 (see above).
(907) Specific absorption parameter values of fr = 0.04, sr = 1 d–1 and ss = 0.0006 d–1(consistent with assignment to default Type S) and fA = 0.0002 are used here for U3O8.
Uranium dioxide (UO2)(908) Uranium dioxide is the final product in the manufacture of nuclear fuel pellets, andis also present as depleted uranium in mixed oxide fuel (MOX). Manufacturing processes of
UO2 differ from one industry to another. Human studies have shown that UO2 can be very
insoluble (Pomroy and Noel, 1981, Price, 1989, Schieferdecker et al., 1985). Experiments in
rats, dogs, monkeys and baboons (Leach et al., 1973, Stradling et al., 1988, Métivier et al.,1992) also support the assignment of UO2 to default Type S. At 30 d after intake by rats andbaboons, the total urinary excretion was 1–4% ILD and lung retention was 60-90% ILD. The
effect of SSA on dissolution has been investigated (Chazel et al., 2000b), but in contrast to
U3O8 (see above), no clear effect was observed. For compounds with SSA varying from 1.0 to
4.4 m2 g–1, fr values were from 0.003 to 0.004.
(909) Ansoborlo et al. (2002) derived absorption parameter values from the results ofstudies in which the biokinetics of uranium were followed for 75 or 90 days after intratracheal
instillation into rats of three forms of UO2: (i) fr = 0.03, sr = 1.25 d–1 and ss = 0.0015 d–1; (ii) fr= 0.01, sr not determined and ss = 0.00049 d–1 (iii) fr = 0.01, sr not determined and ss =0.00058 d–1. Hodgson et al. (2000) derived absorption parameter values from the results of astudy by Stradling et al. (1988) in which the biokinetics of uranium were followed for 315
days after inhalation by rats of two forms of UO2; (non-ceramic) fr = 0.011, sr = 0.95 d–1 andss = 0.00061 d–1; (ceramic) fr = 0.008, sr = 1.3 d–1 and ss = 0.00026 d–1. All but the first ofthese five sets of parameter values are consistent with assignment to default Type S.
Experimental data on ingestion of UO2 by laboratory animals, reviewed by Leggett andHarrison (1995), suggest that absorption in the alimentary tract is about 0.1-0.01 times that of
uranyl nitrate, which is taken here to be 0.02 (see above). Since data on U3O8 (which tends todissolve somewhat more rapidly in the lungs than UO2) suggest that absorption in thealimentary tract is about 0.01 times that of uranyl nitrate, the lower value is applied here.
(910) Specific absorption parameter values of fr = 0.015, sr = 1 d–1 and ss = 0.0005 d–1(consistent with assignment to default Type S) and fA = 0.0002 are used here for UO2.
Vaporised uranium metal(911) A new method for uranium enrichment, based on laser isotopic separation, canproduce three different types of aerosol identified as variable mixtures of Umetal + UO2 +U3O8, with different particle size distributions. Ansoborlo et al. (1998b, 2002) derived
absorption parameter values from the results of studies in which the biokinetics of uranium
were followed for 126 or 168 days after intratracheal instillation into rats of three suchmaterials: (i) fr = 0.36, sr = 1.44 d–1 and ss = 0.0046 d–1; (ii) fr = 0.20, sr = 0.68 d–1 and ss =0.00094 d–1 ;(iii) fr = 0.12, sr = 1.45 d–1 and ss = 0.0026 d–1 (all consistent with assignment todefault Type M).
(912) In view of the wide range of values of ss derived in the study above, these data are
judged to be an insufficient basis to propose specific absorption parameter values andvaporised uranium metal is therefore assigned to Type M.
Uranium ore dust
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11888

(913) Duport et al. (1991) measured the dissolution in simulated lung fluid of long lived
radionuclides in uranium ore dust from Canadian mines (and also in samples of yellowcake
and refined oxides). (For further information see the section below on decay products ofuranium formed in the lungs.) Factors including ore grade (uranium content), particle size,and solution pH were investigated. For high grade ore, measurements were made for up to 60
days, on particles in size ranges that included respirable particles. Results were presented as
undissolved fractions as functions of time, and showed two components, which wereexpressed as Class D (rapid) and Class Y (slow) fractions. For 238U, the rapidly dissolved
fraction was ~0.25 indicating assignment to Type M. No effect of size was observed in total
dissolution over 40 days for particles in size ranges 7–10, 3–7, 1–3 and <1 µm. For low grade
and medium grade ores, measurements were made for 12 days, but only on samples ofrelatively coarse dust, the smallest fraction being <37 µm. For 238U, rapidly dissolved
fractions were greater than those measured in the high grade ores; about 0.33 and 0.5 for low
and medium grade ores respectively.
(914) Bečková and Malátová (2008) measured dissolution for 26 days of 238U, 234U and230
Th in simulated serum ultrafiltrate of uranium ore dust collected on personal air filters in amine in the Czech Republic. Retention (undissolved) was represented by a two-component
exponential function, giving parameter values for 238U of fr = 0.14, sr = 0.49 d–1 and ss = 0.004
d–1 and assignment to Type M. Dissolution of 234U was somewhat faster, as expected due torecoil phenomena: fr = 0.18, sr = 0.49 d–1 and ss = 0.006 d–1. (For further information see thesection below on decay products of uranium formed in the lungs, and the thorium inhalation
section.)(915) Marsh et al. (2011) estimated the following parameter values for dissolution of
uranium from ore dust, based on the results of both Duport et al. (1991) (high grade ore) andthose of Bečková and Malátová (2008): fr = 0.2, sr = 0.8 d–1 and ss = 0.0014 d–1.
(916) For a summary of in vivo and autopsy studies relating to uranium ore dust see thesection below on decay products of uranium formed in the lungs.
Depleted uranium (DU)(917) Depleted uranium, a by-product of the manufacture of enriched uranium for nuclear
reactor fuel, has found a number of applications resulting mainly from its high density, inparticular, in anti-tank munitions, counterweights for aircraft control surfaces and radiation
shielding. DU, typically alloyed with 0.75% titanium is used in ‘kinetic energy penetrators’,rods of the metal fired at very high speed (~1.5 km s–1). On impact with a hard object such asarmour plate, a significant fraction of the penetrator mass may be converted to an aerosol that
could be inhaled by persons in the vicinity or downwind. In vitro tests have shownconsiderable variability in that 1–50% of the respirable material dissolves rapidly, and the rest
very slowly, while X-ray analyses indicate that the uranium is present as a mixture of oxides
including U3O7, U3O8, U4O9, and UO2, but also combinations with other metals (Glissmeyer
and Mishima, 1979, Scripsick et al.,1985a, 1985b, Chazel et al., 2003, Mitchel and Sunder,2004). In vitro dissolution tests carried out by Chazel et al. (2003) gave dissolution parametervalues in the following ranges: fr = 0.47–0.57, sr = 0.06 – 0.07 d–1 and ss = 0.00018 to
0.00034 d–1, giving assignment to Type M.
(918) In the comprehensive Capstone DU Aerosol Study, aerosols formed when DU
rounds penetrated armoured vehicles were used in studies of dissolution in simulated lung
fluid, making measurements over 46 days on a total of 27 samples (Parkhurst et al., 2004a,
2004b; Parkhurst and Guilmette, 2009; Guilmette and Cheng, 2009). Dissolution was fitted
by two- or three-component exponential functions. Based on the two-component fits, there
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was a rapidly dissolving fraction of 1-28% (geometric mean, GM, 12.5%), with an associatedrapid dissolution rate of 0.1-30 d-1 (GM 6 d-1; corresponding half-time, t1/2 = 0.12 d). The
remaining fraction dissolved at a slow rate of 0.0004-0.0095 d-1 (GM 0.0026 d-1: t1/2 = 268 d).
Thus there was considerable variation between samples, especially in the fraction that
dissolved rapidly. There appeared to be some correlation between the initial and final
dissolution rates: the greater the dissolution in the first day, the faster the long term
dissolution rate. Based on extrapolation of the three-component exponential function whereavailable (two-component otherwise), 24 samples would be assigned to Type M and three toType S. Several sets of measurements were made on different stages from the same cascade
cyclone. However, there was no clear trend of dissolution with particle size and in some cases
the back-up filter, with the smallest particles, showed the slowest dissolution. Two
confounding factors were noted: (1) cyclone cut-offs are not sharp, so there was considerable
overlap in size distribution between stages (2) scanning electron microscope examination
showed great heterogeneity of particle composition, shape etc.
(919) Mitchel and Sunder (2004) followed urinary excretion of uranium for 7 days after
intratracheal instillation into rats of the <50-µm fraction of dust obtained from impact of DU
munitions on armour plate. Results indicate that about 10% ILD dissolved during 7 days,
about half of it within 1 day. However, the large size suggests that the material was fromsurface deposits rather than air samples, and may not be representative of dust that might beinhaled.
(920) If large pieces of uranium metal are subjected to fire (e.g. in a burning vehicle oraircraft crash - generally depleted uranium is used in applications which require only the nonfissile properties of uranium) they will gradually oxidise and some of the oxide may bedispersed and inhaled. In vitro tests have shown that 0.5–10% of the respirable material
dissolves rapidly, and the rest very slowly, while X-ray analyses indicate that most of theuranium is present as U3O8 (Mishima et al., 1985, Elder and Tinkle, 1980, Scripsick et al.,1985a, OSAGWI, 2000). Default Type M should be assumed.
(921) Overall, the available data show that the dissolution and lung absorption ofparticulate DU, whether formed by the impact of kinetic energy penetrators, or in fires, is veryvariable. It is therefore judged to be inappropriate to propose specific absorption parametervalues and DU is therefore assigned to default Type M.
Irradiated fuel fragments(922) Following an accidental release from a nuclear reactor, fission and activation
products may be present in fragments of irradiated fuel, of which the matrix is predominantly
uranium dioxide (Devell, 1988, Begichev et al., 1989, Toivonen et al., 1992). In studies of thein vitro dissolution of particles released from the Chernobyl accident, seven out of ten ofwhich consisted mainly of uranium (Cuddihy et al., 1989), the data obtained were consistent
with assignment of all the γ-emitting radionuclides to Type M.
Decay products of uranium formed in the respiratory tract(923) Decay schemes of uranium isotopes in the natural decay series: 234U, 238U and 235U,
are described in Figure 15-1 and Figure 15-2. The 232Th decay series is shown in the thorium
inhalation section (Figure 14-1): it is relevant to 232U, which decays to 228Th, a descendent of
232
Th.

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Uranium-234

Uranium-238αα 240,000 years
4.5 billion years
β 1.2 minutes
Protactinium-234m
βNotes:The symbols α and β indicate alpha and beta
decay, and the times shown are half-lives.

24 daysThorium-230

Thorium-234

αAn asterisk indicates that the isotope is also
a significant gamma emitter.

77,000 years

Uranium-238 also decays by spontaneous
fissionRadium-226
α1,600 years

Radon-222
α

3.8 daysα

Polonium-210

Polonium-214

Polonium-218

α

3.1 minutesββ

20 minutesβ
27 minutes

22 years
Lead-206 (stable)

Lead-210

Lead-214*

11936
11937
11938
11939
11940

140 days

5.0 days

Bismuth-210

Bismuth-214*βα160 microseconds

Figure 15-1. Natural decay series: Uranium-238

Notes:The symbols α and β indicate alpha and beta
decay, and the times shown are half-lives.

Uranium-235*α

700 million years

An asterisk indicates that the isotope is also
a significant gamma emitter.

Protactinium-231*βα33,000 years

26 hours
Thorium-227*

Thorium-231

βActinium-227
α

22 years(99%)α

19 daysRadium-223*
22 yearsαβ
11 days(1%)
22 minutes

Francium-223*

Radon-219*
α4.0 seconds

Polonium-215
α

1.8 milliseconds
Bismuth-211*β

α2.1 minutes

36 minutes

Lead-211*

11941
11942
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11945
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11950

Lead-207 (stable)
β4.8 minutes

Thallium-207

Figure 15-2. Natural decay series: Uranium-235(924) The general approach to treatment of decay products formed in the respiratory tract
is described in Part 1, Section 3.2.3. In summary, it is expected that generally the rate at
which a particle dissociates is determined by its matrix, and hence the physico-chemical formof the inhaled material. It is recognised that for decay products formed within particles byalpha emission, recoil of the daughter nucleus from the alpha emission expels some of the
decay product from the particle. In the case of decay chains, this will result in successively
lower activities of members compared to the parent retained in relatively insoluble particles.

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11991
11992
11993
11994
11995
11996
11997
11998

Experimental evidence relating to this is described in the section on relatively insoluble (TypeS) forms of thorium formed in the respiratory tract. However, it was considered impracticalto implement loss of decay products by alpha recoil in the calculation of dose coefficients andbioassay functions in this series of documents. (For further information see Part 1, Section
3.2.3.) Nevertheless, this phenomenon should be borne in mind, especially when using decay
products to monitor intakes and doses of the parent, which can be applicable to uranium.
(925) Exceptions are made for noble gases formed as decay products, which are assumed
to escape from the body directly, in addition to other routes of removal. For calculation
purposes it is assumed that radon formed as a decay product within the respiratory tract
escapes from the body at a rate of 100 d–1, in addition to other routes of removal. For further
information see the section on relatively insoluble (Type S) forms of thorium formed in the
respiratory tract.
(926) It is expected that the behaviour of soluble (e.g. Type F) material in the respiratory
tract would depend on its elemental form, i.e. that of the decay product. Nevertheless, forsimplicity, in this series of documents the absorption parameter values of the parent are, by
default, applied to all members of the decay chain formed in the respiratory tract.
(927) The formation of thorium as a decay product can be of particular importance in thiscontext, because there can be significant long-term retention of thorium in the lungs
following its deposition in soluble form (see thorium inhalation section). Conversely,
important decay products of thorium, notably radium and lead, in soluble forms, are (likeuranium) relatively readily absorbed from the respiratory tract into the systemic circulation.
Studies specifically comparing the behaviour of uranium with that of its decay products are
summarised here, although it should be noted that the thorium was mainly administered withthe uranium, rather than formed from decay of uranium in the respiratory tract. For more
information, see also the sections on thorium, radium, polonium, lead and bismuth, relating to
the behaviour of their decay products formed in the respiratory tract.
Relatively soluble (Type F) forms(928) As noted above, Ballou et al. (1986) studied the biokinetics of 232U and 233U in rats
after inhalation of uranyl nitrate aerosols. For the main studies, the uranium was freshly
separated from its decay products, and measurements were not made of decay products
formed within the body. Uranium-233 has a long half-life (1.6x105 years), but that of 232U is
only 74 years and the authors recognised that assessment of doses from occupational exposure
to 232U needed to take account of the behaviour of its decay products, especially 228Th. A
complementary experiment was carried out in which tissue distributions of 232U, 228Th, 224Ra,
212
Pb, 212Bi and 208Tl were measured at 24 hours after intratracheal instillation into rats of232
U nitrate with its decay products. Although measurements of 228Th, 224Ra, and perhaps
212
Pb, were mainly of material administered with the parent 232U, rather than formed from its
decay in the lungs, it is reasonable to assume similar behaviour. (The physical half-lives of212
Bi and 208Tl are so short, 61 minutes and 3 minutes respectively, that measurements madeat 24 hours would mainly be of activity formed in situ.) Lung retention was 7.9% ILD for
232
U, 52% ILD for 228Th, and about 2-3% ILD for the other decay products measured,reflecting the high lung retention of thorium, and relatively rapid lung clearance of radium
and lead observed in other studies in which soluble forms were administered. Similarly, thedistribution between liver, skeleton and kidneys of 232U, 228Th, 224Ra and 212Pb reflected theelemental forms. The distributions of 212Bi and 208Tl were similar to those of 212Pb,
presumably because of their short physical half-lives: whatever their distribution in vivo, theywould tend to equilibrium between dissection and measurement. Ballou et al. noted that the299

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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12000
12001
12002
12003
12004
12005
12006
12007
12008
12009
12010
12011
12012
12013
12014
12015
12016
12017
12018
12019
12020
12021
12022
12023
12024
12025
12026
12027
12028
12029
12030
12031
12032
12033
12034
12035
12036
12037
12038
12039
12040
12041
12042
12043
12044
12045
12046

greater retention of 228Th in the lungs and deposition in skeleton than of the 232U, suggested
that assessments based on the assumption of shared kinetics would significantly
underestimate doses.
(929) Stradling et al. (2005) followed the biokinetics of uranium and thorium for 3 months
after intratracheal instillation into rats of the nitrates, given separately, or together at uranium:
thorium mass ratios of 5x106:1 or 50:1. Their behaviour when administered separately was as
expected from other studies: by 1 day ~80% ILD of uranium but only ~30% ILD of thorium
had been absorbed into blood. The behaviour of thorium was not significantly affected by thepresence of uranium when they were administered together (for further information see
thorium inhalation section).
Relatively insoluble (Type M or S) forms(930) Hill (1962) noted the disequilibrium between the early long-lived members of theuranium decay series measured in a lung sample from a uranium miner, although they were
probably close to equilibrium in the uranium ore to which he was exposed. The concentrationof 230Th was about twice, and that of 226Ra about half, that of 238U or 234U, suggesting
selective removal of radium and uranium compared to thorium.
(931) Stuart and Beasley (1967) followed the biokinetics of uranium (238U + 234U) andthorium (228Th) for up to 4 months after repeated inhalation by rats of uranium ore dust
(pitchblende, 25% U3O8, with uranium and thorium in secular equilibrium) over an 8-weekperiod. Faster clearance from the lungs of uranium than thorium was observed: at 1 week
after the end of exposures the thorium activity was 2 – 3 times that of 238U or 234U. Stuart andJackson (1975) similarly found 230Th concentrations were several times those of 238U in thelungs and lymph nodes of dogs at 2 weeks or 15 months after repeated inhalation of the same
uranium ore (Cross et al., 1982). They also reported that thorium concentrations in the lungs
were about twice those of uranium in hamsters one year after repeated inhalation of carnotite
ore dust (4% U3O8, with uranium and thorium in secular equilibrium), and several times
higher in dogs after several years of daily inhalation exposure. Thus even though the material
was relatively insoluble, and the thorium was present as a minor component by mass, its
slower absorption from the lung than that of uranium could be observed.
(932) Fisher et al. (1983) measured significantly higher activity levels of 234U and 238U
than of the daughter product 230Th in both urine and fecal samples obtained from active
uranium millers, indicating that uranium in the inhaled ore dust was cleared from the bodywith a shorter biological half-time than the daughter product 230Th. Assessment of lungclearance from the results is not straightforward, especially given the chronic and continuing
exposures. Higher urinary excretion of uranium than of thorium would be expected even if
absorption from the lung were at similar rates, because of the higher urinary excretion ofsystemic uranium. For both elements fecal clearance dominated, and given the high urinary
excretion of systemic uranium, this suggests greater lung clearance by particle transport thanby absorption to blood. The lower fecal excretion of thorium than of uranium suggests a
lower particle transport rate, and hence that there is binding of thorium released in the lungs
by dissolution. However, it was recognised by the authors that other sources of fecal excretionof uranium (dietary intakes, exposure to refined uranium which is depleted in thorium) could
not be excluded.
(933) In contrast, Wrenn et al. (1983) measured 230Th concentrations similar to those of234
U in the lungs of five uranium miners (average 230Th/234U ratio 1.1, range 0.54–2.6). They
noted that this was surprising in view of the results of the reported disequilibrium in dogs
chronically exposed to carnotite (see above). An interlaboratory comparison was conducted,
300

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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12048
12049
12050
12051
12052
12053
12054
12055
12056
12057
12058
12059

which showed that the difference was not due to differences in radiochemical methods (Singhet al., 1986a). In a later study (Singh et al., 1987) the same group found ratios of 1.5–3.5 inthe lungs of three uranium miners and 1.1–1.3 in the lungs of two uranium millers: they
concluded that overall, dissolution in the human lungs of uranium and thorium in uranium ore
dust was similar.
(934) As noted above, Duport et al. (1991) measured the dissolution in simulated lung
fluid of long lived radionuclides in uranium ore dust from Canadian mines. For high gradeore, measurements were made for up to 60 days, on particles in size ranges that included
respirable particles. For 238U, 230Th, 226Ra, and 210Pb, the rapidly dissolved fractions were0.25, 0.15, 0.12 and 0.28 respectively. Marsh et al, 2011, fitted two-component exponentialfunctions to the data (un-dissolved fractions) and obtained the following HRTM parametervalues:Nuclide
230
Th
226
Ra
210
Pb

12060
12061
12062
12063
12064
12065
12066
12067
12068
12069
12070
12071
12072
12073
12074
12075
12076
12077
12078
12079
12080
12081
12082
12083
12084
12085
12086
12087
12088
12089
12090

fr
0.14
0.11
0.26

sr (d–1)
4.6
7.3
3.9

ss (d–1)
0.00070.00040.001(935) For these radionuclides, no effects of size were observed in total dissolution over 40days for particles in size ranges 7–10, 3–7, 1–3 and <1 µm. For low grade and medium gradeores, measurements were made for 12 days, but only on samples of relatively coarse dust, thesmallest fraction being <37 µm. For 238U, rapidly dissolved fractions were higher (0.33 and
0.5 for low and medium grade ores) than those measured in the high grade ores. However, forother radionuclides the fractions were lower: 0.07 for 226Ra, and <0.01 for 210Pb.
Measurements were also made for 232Th in low grade ore and 210Po in low and medium gradeores, and much lower fractions obtained, 0.01, 0.00 and 0.005 respectively. Consistentdifferences in dissolution between uranium and its decay products were not apparent.
(936) As noted above, Bečková and Malátová (2008) measured dissolution for 26 days of
238
U, 234U and 230Th in simulated serum ultrafiltrate of uranium ore dust collected on personal
air filters in a mine in the Czech Republic. Moderate dissolution of both uranium isotopes
was observed, with fr = 0.14 for 238U and 0.18 for 234U, but no dissolution of 230Th was
detected.
(937) Griffith et al. (1980) developed a model to describe the retention of 232U and its
decay products, in the lungs following inhalation in ThO2 or UO2 particles. In addition tochemical dissolution, they considered recoil emanation of daughter product nuclei by alphaparticle decay, and diffusion emanation of 220Rn from particles. In complementary
experiments, Coombs and Cuddihy (1983) measured the fraction of 228Th escaping by recoil
and the fraction of 220Rn escaping by diffusion from size-fractionated samples of ThO2 anduranium oxide (mixture of UO2.2 and U3O8) containing 1% 232U. For further information onthese and other studies relating to recoil emanation of decay products and to loss of radon
formed in the respiratory tract see the section on decay products of thorium formed in the
respiratory tract.
Rapid dissolution rate for uranium(938) Studies on the uranium compounds which are most rapidly absorbed from the lungs(uranium hexafluoride and uranyl tri-butyl-phosphate) give values of sr of about 10 d–1, which
is applied here to all Type F forms of uranium in the absence of material-specific data.

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DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12091
12092
12093
12094
12095
12096
12097
12098
12099
12100
12101

Extent of binding of uranium to the respiratory tract(939) Experimental evidence suggests that there is little binding of uranium to therespiratory tract. Cooper et al. (1982) and Ellender (1987) followed the behaviour of 233U
after instillation of uranyl nitrate and bicarbonate into the pulmonary region of the lungs ofrats. Cooper et al. (1982) found that less than 2% ILD remained at 7 days. Ellender (1987)
gave more information for the nitrate, for which about 8% ILD remained at 1 d and 3% at 30
d. Detailed analysis, however, indicates that clearance over this period was mainly by particle
transport, and that the results did not provide evidence for binding of uranium (Hodgson, etal., 2000). It is therefore assumed that for uranium the bound state can be neglected, i.e. fb =
0.0.

302

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION

Table 15-2. Absorption parameter values for inhaled and ingested uranium

12102
12103

Inhaled particulate materials
Specific parameter valuesb
Uranyl Tri-Butyl-Phosphate (U-TBP)Uranyl nitrate, UO2(NO3)2
Uranium peroxide hydrate UO4Ammonium diuranate, ADU
Uranium trioxide UO3Uranium tetrafluoride UF4
Triuranium octoxide U3O8
Uranium dioxide UO2Uranium aluminide UAlX

Absorption
parameter Absorption fromvaluesathealimentaryfrsr (d–1) ss (d–1)
tract, fA d
0.97
0.9
0.9
0.8
0.8
0.6
0.04
0.015
c

Default parameter valuesd,eAbsorption
Assigned forms
Type
F
Uranium hexafluoride, UF6
1
M
Uranyl acetylacetonate; DU 0.2
aerosols from use of kinetic
energy penetrators; vaporized
U metal; all unspecified
formsfS—
0.01
Ingested materials
Soluble forms (Type F)–
Relatively insoluble forms (as assigned to –Types M and S for inhalation)
12104
12105
12106
12107
12108
12109
12110
12111
12112
12113
12114
12115
12116
12117
12118
12119
12120
12121
12122
12123
12124
12125

12
3
0.9
0.7
1
0.15
1
1
c

0.002
0.005
0.02
0.02
0.01
0.005
6x10-45x10-4
c

0.02
0.02
0.01
0.02
0.01
2x10-42x10-42x10-4
0.002

10
3

0.005

0.02
4x10-33

1x10-42x10-4

–
–

–
–

0.02
0.002

a

It is assumed that for uranium the bound state can be neglected, i.e. fb = 0.0. The value of sr for Type F formsof uranium (10 d–1) is element-specific. The values for Types M and S (3 d–1) are the general default values.
b
See text for summary of information on which parameter values are based, and on ranges of parameter values
observed for individual materials. For uranium specific parameter values are used for dissolution in the lungs,
and where information is available for absorption from the alimentary tract. For other materials, the default
value of fA is used (footnote d).
c
See text: sp = 1x10-4 d–1, spt = 4x10-3 d–1, st = 4x10-3 d–1, with fA taken to be 0.002.
d
For inhaled material deposited in the respiratory tract and subsequent cleared by particle transport to thealimentary tract, the default fA values for inhaled materials are applied: i.e. the (rounded) product of fr for theabsorption Type (or specific value where given) and the fA value for ingested soluble forms of uranium (0.02).
eMaterials (e.g. UF6) are listed here where there is sufficient information to assign to a default absorption Type,but not to give specific parameter values (see text).
f
Default Type M is recommended for use in the absence of specific information, i.e. if the form is unknown, or
if the form is known but there is no information available on the absorption of that form from the respiratory
tract.

15.2.2. Ingestion(940) Data on the absorption of uranium have been reviewed by Wrenn et al. (1985),
Harrison (1991), Leggett and Harrison (1995) and in ICRP Publication 69 (1995).
(941) In the first controlled human study involving more than one subject, Hursh et al.
(1969) administered uranyl nitrate to four hospital patients. The data obtained were taken to303

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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12127
12128
12129
12130
12131
12132
12133
12134
12135
12136
12137
12138
12139
12140
12141
12142
12143
12144
12145
12146
12147
12148
12149
12150
12151
12152
12153
12154
12155
12156
12157
12158
12159
12160
12161
12162
12163
12164
12165
12166
12167
12168
12169
12170
12171
12172
12173

suggest fractional absorption in the range 0.005 - 0.05. Leggett and Harrison (1995) haveinterpreted the data as suggesting absorption of 0.004, 0.01, 0.02 and 0.06, respectively, forthe four subjects. Wrenn et al., (1989) estimated absorption in twelve normal healthy adultvolunteers given drinking water high in uranium. On the basis that 40 - 60% of absorbed U
was excreted in the urine in the first three days, rather than the author’s assumption of 79%,
Leggett and Harrison (1995) concluded that mean absorption was 0.01-0.015, maximum
absorption was in the range 0.02-0.04, and that six subjects absorbed less than 2.5x10-3.
Harduin et al., (1994) reported results for the absorption of U from drinking water either
administered on one day or over 15 days. The data for acute administration suggested
absorption of 0.005-0.05 with an average value of 0.015-0.02. The data for 15-day
administration suggested absorption of 0.003-0.02 and average absorption of 0.01-0.015. In
another in situ study, the gastro-intestinal absorption factor was determined for 50
participants ingesting uranium at natural levels in drinking water and food. The participants,
ranged in age from 13 to 87 years were selected from either a Canadian area with naturallyhigh (2-780 µg.L-1) or low (<1µg.L-1) uranium levels. The distribution of f1 values obtained
was non-Gaussian with a range of 0.001 to 0.06 and a median of 0.009 (Zamora et al, 2002).
These values were not gender sensitive and independent of age at the time of the study,
duration of exposure and total uranium intake. Similar results have also been obtained in a
number of dietary balance studies (Larsen and Orlandini, 1984; Spencer et al., 1990; Wrennet al., 1989; Leggett and Harrison, 1995).
(942) Data from animal studies provide information on the relative uptake of U ingested indifferent chemical forms, showing that absorption is strongly dependent on the solubility of
the compound. Measurements have been made in rats, hamsters, rabbits, dogs and baboons(reviewed by Wrenn et al., 1985; Harrison, 1991; Leggett and Harrison, 1995). Absorption
appears to be greatest for U ingested as UO2(NO3)2.6H2O, U-TBP, UO2F2 or Na2U2O7,
roughly half as great for UO4 or UO3, and 1 - 2 orders of magnitude lower for UCl4, U3O8,
UO2 and UF4. It should be noted, however, that the solubility of some poorly soluble U
compounds can vary substantially with thermal history as well as particle size (Cooke andHolt, 1974). Thus, greater absorption as UO2 in hamsters than rats and dogs, could reflectsolubility of the preparation of UO2 rather than just species differences. A number of studies
have shown that absorption is substantially greater in fasted than fed animals. For example,
Bhattacharyya et al., (1989) found that uptake was increased by an order of magnitude in miceand baboons deprived of food for 24 h prior to U administration. Sullivan (1980) reported a 2– 4 fold increase in U absorption in rats given U nitrate after a 24 hour fast.
(943) In Publication 30 (ICRP, 1979), an f1 of 0.05 was recommended for water soluble
inorganic forms of U(VI) and a value of 0.002 for U(IV) in relatively insoluble compounds
such as UF4, UO2 and U3O8. In Publication 69 (ICRP, 1995), an f1 of 0.02 was adopted for
dietary intakes of U on the basis of human data as reviewed by Wrenn et al., (1985), Harrison(1991) and Leggett and Harrison (1995). The available human and animal data indicate that avalue of 0.02 is also appropriate for occupational exposures to more soluble inorganic forms,
including UO2(NO3)2.6H2O, UO2F2 and Na2U2O7.
(944) In this report, an fA value of 0.002 is adopted for the fractional absorption ofrelatively insoluble compounds (e.g. UO2, U3O8) and an fA value of 0.02 is adopted for allother more soluble chemical forms (Table 15-2).
15.3.

Systemic Distribution, Retention and Excretion

15.3.1. Summary of the database304

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12174
12175
12176
12177
12178
12179
12180
12181
12182
12183
12184
12185
12186
12187
12188
12189
12190
12191
12192
12193
12194
12195
12196

Controlled studies on human subjects(945) The systemic biokinetics of uranium has been investigated in three human injection
studies known as the Boston study, the Rochester study, and the Terepka study.
(946) The Boston study (Struxness et al., 1956; Bernard and Struxness, 1957; Luessenhop
et al., 1958) involved 11 patients, ages 26-63 y, in the terminal phases of diseases of thecentral nervous system. Most of the subjects were comatose at the time of injection. Uranyl
nitrate solutions enriched with 234U and 235U were administered to Subjects 1-6 and Subjects
9-11 by intravenous injection. Subjects 7 and 8 received intravenous injections of tetravalenturanium as UCl4. The mass of administered uranium was varied from one subject to anotherbut ranged up to about 1 mg/kg. The mass of injected uranium is known only approximately
for Subjects 2, 9, 10 and 11. In some cases, several bone biopsy samples were taken from theanterior tibia during the first day or two after injection. Extensive measurements of uranium
in blood and excreta were made over the first several weeks or months after injection. Urinary
uranium measurements were made over several months in some of the Boston subjects andextended to times >1 y for one subject. Autopsy samples were obtained from various bones
and soft tissues of subjects dying at times from 2.5 d to 4.5 months after injection and fromone subject dying 566 d after injection.
(947) Selected data from the Boston study are summarised in Table 15-3. The range ofvalues given for bone indicate the lower and upper bounds derived from different
assumptions regarding the portion of the skeleton represented by samples collected at
autopsy.
Table 15-3. Summary of results for eight of the Boston subjects, based on data ofStruxness et al. (1956) and Bernard and Struxness (1957), and logbooks from the Boston
study (after Leggett, 1994).
Subject numberTime to death (d)Urinary U, day 1 (%)
Kidney (%)
Bone (%)
Liver (%)
Other soft tissues (%)

12197
12198
12199
12200
12201
12202
12203
12204
12205
12206
12207
12208
12209
12210

1
2.5
59
14
8-12
1.5
6

6
18
49
6
4-13
1.0
4

9
25
~80
1.7
1.5-2.5
0.2
1

11
28
~60
1.6
2-3
0.05
2

2
74
78
0.6
1.2-2
0.2
1.5

10
94
~80
0.8
2.5-3
0.01
2.5

5
139
67
1.0
0.5-0.7
0.15
0.5

3
566
84
0.3
1.1-1.7
0.05
0.3(948) The poor physical condition of the Boston subjects limits the confidence with which
the data can be taken to represent the typical biokinetics of uranium. Struxness et al. (1956)
pointed out that the bed-ridden condition of these subjects indicated a negative calcium
balance, which might "hasten the removal of uranium from the skeleton". Also, the subjects
were given relatively high masses of uranium. Animal studies indicate that administration ofhigh masses of uranium will result in elevated uptake and retention in kidneys, among several
potential effects on biokinetics (Bernard and Struxness, 1957; Leggett, 1989; 1994). A third
difficulty is that the post-mortem data are not sufficiently detailed in some cases to allow a
close determination of the total uranium content of some organs or tissues, particularly theskeleton.
(949) The Rochester study involved two female and four male subjects, ages 24-61 y,chosen because they had reasonably good kidney function and their urine was free of protein(Bassett et al., 1948). These subjects were hospital patients but were ambulatory. Subjects 1-

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DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12211
12212
12213
12214
12215
12216
12217
12218
12219
12220
12221
12222
12223
12224
12225
12226
12227
12228
12229
12230
12231
12232
12233
12234
12235
12236
12237
12238
12239
12240
12241
12242
12243
12244
12245
12246
12247
12248
12249
12250
12251
12252
12253
12254
12255
12256

6, respectively, suffered from rheumatoid arthritis, cirrhosis of the liver, chronic
undernutrition, alcoholism, unresolved pneumonia, and pulmonary fibrosis plus gastric ulcer.
The subjects received intravenous injections of uranyl nitrate solutions enriched with 234U and235
U. Administered masses ranged from 6.3 to 70.9 μg U/kg. Total urine and faecal
collection was made for up to 16 d, and several blood samples were taken.
(950) Terepka and co-workers (Terepka et al., 1964; Hursh and Spoor, 1973) investigatedthe possibility of evaluating bone disorders based on the level of retention of intravenously
injected uranium. They injected hexavalent uranium (30 μg/kg) into three control patientsand seven patients with various bone disorders (Paget's disease, hyper- or
hypoparathyroidism, osteomalacia, or senile osteoporosis). Some patients were investigatedbefore and after oestrogen or parathyroid extract treatments. Urinary excretion of uranium
was measured for at least 6 d in each subject. Subjects with osteomalacia and Paget’s disease
showed radically reduced urinary uranium compared with controls, presumably due toradically increased uptake of uranium by the skeleton. Cumulative urinary uranium over 6 d
was similar in controls and subjects with osteoporosis or hyper- or hypoparathyroidism.
Occupational and environmental studies(951) Additional information on the biological fate of uranium in humans is provided bypost-mortem measurements of uranium in tissues of occupationally and environmentally
exposed subjects (Donoghue et al., 1972; Campbell, 1975; Roberts et al., 1977; Igarashi et al.,
1985; Fisenne and Welford, 1986; Sing et al., 1986, 1987; Kathren et al., 1989; Russell andKathren, 2004). Such studies provide information on the long-term distribution of uranium inthe human body. For example, the collective data from these studies suggest that the skeleton
typically contains 15-50 (median, ~30) times as much uranium as the liver, and the kidneys
typically contain 0.2-0.6 (median, ~0.5) times as much uranium as the liver at times remotefrom the start of exposure. Some limitations of the post-mortem data for modelling purposes
are the small numbers of subjects examined in most studies; uncertainties in the exposure
histories of those subjects; uncertainties in estimates of total-organ contents of the subjects
based on small samples of tissue, particularly skeletal tissues; and, in some cases, unreliable
techniques for determining low concentrations of uranium in tissues or fluids.
Animal studies(952) The biokinetics of uranium has been studied in baboons, dogs, rabbits, rats, mice,monkeys, sheep, and other animal species (see reviews by Durbin, 1984; Leggett, 1994;
ICRP, 1995). As indicated in the following discussion of model parameter values, data fromseveral animal studies were used in the development of parameter values for the systemic
model described below. The animal data helped to fill gaps in the human data and inselection of some parameters were given heavier weight than questionable data for humansubjects. In addition to uncertainties regarding interspecies extrapolation of results, theanimal data have many of the same problems that complicate the human studies. For
example, most animal studies involved administration of relatively high masses of U; there
was often limited sampling of tissues, particularly bone and massive soft tissues such asmuscle, fat, and skin; and some studies involved small numbers of animals. When potentiallysignificant differences in numerical results were indicated by results of different animalstudies, preference was generally given to baboons or dogs over rats or other small animals,
and to results involving uptake of relatively low masses of uranium.

306DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12257
12258
12259
12260
12261
12262
12263
12264
12265
12266

12267
12268
12269
12270
12271
12272
12273
12274
12275
12276
12277

15.3.2. Biokinetic model for systemic uranium(953) The biokinetic model for systemic uranium used in this report is the model for adults
adopted in ICRP Publication 69 (1995) and applied in ICRP Publication 68 (1994a) toworkers. The model structure (Figure 15-3) is the generic structure for elements that follow
the movement of calcium in bone. Although the chemical analogy between UO22+ and Ca2+ is
not strong in terms of affinity constants for mineral ligands (Ansoborlo et al., 2006), thebehaviour of uranium in the skeleton shows qualitative similarities to that of calcium.

Figure 15-3. Structure of the model for systemic uranium.

(954) Parameter values for the worker are listed in Table 15-4. Primary databases andassumptions underlying parameter values are summarized below. Additional details andreferences can be found in an article by Leggett (1994). In that article parameter values are
first discussed for a relatively detailed model with regard to the time dependent kinetics ofuranium in blood and kidneys and then are adjusted to the less detailed generic model
structure for calcium-like elements.

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12278

Table 15-4. Transfer coefficients in the model for systemic uranium.
From
PlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaPlasmaST0
RBC
Kidneys (Urinary path)
Kidneys (Other kidney tissue)
Liver 1
Liver 1
Liver 2
ST1
ST2
Trabecular bone surface
Trabecular bone surface
Cortical bone surface
Cortical bone surface
Trabecular bone volume
Cortical bone volume
Excha trabecular bone volume
Exch trabecular bone volume
Exch cortical bone volume
Exch cortical bone volumeaExchangeableb
Non-exchangeable
12279
12280
12281
12282
12283
12284
12285
12286
12287
12288
12289
12290
12291
12292

To
ST0
RBC
Urinary bladder content
Kidneys (Urinary path)
Kidneys (Other kidney tissue)
Right colon content
Liver 1
ST1
ST2
Trabecular bone surface
Cortical bone surface
PlasmaPlasmaUrinary bladder content
PlasmaPlasmaLiver 2
PlasmaPlasmaPlasmaPlasmaExch trabecular bone volume
PlasmaExch cortical bone volume
PlasmaPlasmaTrabecular bone surface
Nonexchb trabecular bone volume
Cortical bone surface
Nonexch cortical bone volume

Transfer rate (d-1)
10.5
0.245
15.43
2.94
0.0122
0.122
0.367
1.63
0.0735
2.04
1.63
8.32
0.347
0.099
0.00038
0.092
0.006930.000190.03470.000019
0.06930.06930.06930.06930.000493
0.0000821
0.01730.005780.01730.00578

Blood clearance(955) There is rapid loss of uranium from the circulation in the first few minutes after
injection due to high rates of filtration by the kidneys and diffusion into extracellular fluid.
The rate of disappearance declines as uranium returns from the extracellular spaces to bloodand some uranium attaches to red blood cells. In human subjects given uranyl nitrate
intravenously, median retention in blood was about 25% at 5 min, 10% at 2 h, 5% at 5 h, 1%
at 20 h, and <0.5% at 100 h, but inter-subject variation was high (Bassett et al., 1948; Bernard
and Struxness, 1957). Blood clearance rates observed in baboons (Lipsztein, 1981) and dogs
(Rowland and Farnham, 1969) are similar to those determined in human subjects.
(956) Limited measurements on human blood containing environmental levels of uranium
indicate that a substantial portion of uranium in blood is associated with red blood cells(Leggett, 1994). Measurements of intravenously injected uranium in plasma and red blood
cells of baboons showed that red blood cells contained on average about 10% of circulating

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12299
12300
12301
12302
12303
12304
12305
12306
12307
12308
12309
12310
12311
12312
12313
12314
12315
12316
12317
12318
12319
12320
12321
12322
12323
12324
12325
12326
12327
12328
12329
12330
12331
12332
12333
12334
12335
12336
12337
12338
12339
12340

uranium after 2 hours, 25% after 6 hours, 80% after 1 day and at least 50% from 1 - 49 days
(Lipsztein, 1981). These data indicate that about 0.5 – 1% of uranium from plasma attaches to
red blood cells and is returned to plasma with a half-time of about 1 day (Leggett, 1994).
(957) Morrow et al. (1982) estimated that soft tissues of beagles given intravenous
injections of UO2F2 contained about 24% of the administered amount after 24 hours and 4%
after 48 hours. This presumably reflects a high rate of transfer of uranium from blood to
extracellular fluids and subsequent return to the circulation over a period of hours.
(958) In the present model, plasma is taken to be a uniformly mixed pool from whichuranium is removed at a rate of 35 d-1, with 30% going to a soft-tissue compartment called
ST0 that returns uranium to blood with a half-time of 2 h. Thus, the transfer coefficient fromplasma to ST0 is 35 d-1 x 0.3 = 10.5 d-1 and from ST0 to plasma is ln(2) / 2 h = 8.32 d-1.
Resulting model predictions are in reasonable accord with data for blood clearance in the
Boston subjects, animal data on binding of uranium to red blood cells (Lipsztein, 1981), andthe early rise and fall of uranium in soft tissues of beagles (Morrow et al. (1982)).
Urinary excretion and renal retention(959) Data from the human injection studies indicate that typically about two-thirds ofintravenously injected uranium is excreted in the first 24 hours and a further 10% over the
next 5 days. Similar results were obtained for baboons and beagle dogs. The human andanimal data indicate that most of the remaining uranium is excreted over a period of a few
months, but a few percent of the amount injected may be retained for a period of years(Bernard et al., 1957; Struxness et al., 1956; Luessenhop et al., 1958; Stevens et al., 1980;
Sontag, 1984).
(960) A substantial fraction of uranium filtered by the kidneys is temporarily retained in
the renal tubules before passing in the urine to the urinary bladder. Morrow et al. (1982)
estimated that the kidneys of beagle dogs contained 44% of uranium reaching blood at 6hours after inhalation of UO2F2 and 16% after 24 hours. At 1 – 3 days after inhalation or
injection of soluble forms of uranium, the kidneys of humans, dogs and rats contained 12 –25% of the amount entering blood (Bernard and Struxness, 1957; Muir et al., 1960; Jones,
1966; Stevens et al., 1980; Morrow et al., 1982). Durbin (1984) reviewed data on theretention of uranium in the kidneys of humans, beagles, rats and mice and concluded that 92 –95% of the renal content at 1 day was lost with a half-time of 2 – 6 days and the remainder
was lost with a half-time of 30 – 340 days. Interpretation of the data is complicated byindications that retention in the kidneys depends on the mass of uranium administered(Leggett, 1994).
(961) In the present model, urinary excretion is assumed to occur in part from directtransfer from plasma to the urinary bladder contents, accounting for 63% of uranium leaving
the circulation, and in part after temporary retention in renal tubules, accounting for 12% ofuranium leaving the circulation. The half-time of retention in the renal tubules is taken to be 7
days. The model also includes other kidney tissues which are assumed to receive 0.05% ofuranium leaving the circulation, retained with a half-time of 5 years. These parameter values
were chosen to be consistent with data on urinary excretion and renal retention of uranium,including data for the relative retention in kidneys and liver in occupationally andenvironmentally exposed humans. Parameter values for Kidney 2 were based to a large extent
on retention data on baboons injected with tracer quantities of uranium (Neton et al., 1979,
Lipsztein 1981, Bhattacharyya et al., 1989) and data on dogs administered low to moderatemasses of uranium (Tannenbaum 1951, Fish and Bernard 1961). However, the model was
required to remain broadly consistent with data on humans and dogs exposed to relatively
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12342
12343
12344
12345
12346
12347
12348
12349
12350
12351
12352
12353
12354
12355
12356
12357
12358
12359
12360
12361
12362
12363
12364
12365
12366
12367
12368

high masses of uranium.
(962) Model predictions of short-term urinary excretion of uranium are compared in Figure15-4 with data from the human injection studies. The model was not designed to reproduce
the central values of the observations for these subjects at later times due to the poor physicalconditions of most of the subjects and the high variability of the data. Model predictions ofdaily urinary uranium are within the wide range of observations at all times but are generally
higher than central values from the injection studies at times greater than a few days after
injection. Essentially, predictions of urinary uranium at remote times are driven by parametervalues for uptake and removal of uranium by individual tissues, particularly the skeleton,
which is expected to contain most of the retained uranium by a few weeks after uptake.
Faecal excretion(963) Faecal excretion accounted for less than 1% of total excretion in the human injection
studies discussed above (Leggett, 1994; ICRP 1995a). Similar results were obtained forbaboons (Lipsztein, 1981). In beagles, an estimated 2 – 5% of injected uranium was excreted
in the faeces in the first 2 weeks (Stevens et al., 1980; Morrow et al., 1982). In the ICRP
model, faecal excretion is included as 0.5% of uranium leaving the circulation entering theright colon.
Liver retention(964) The assumptions for uranium retention in the liver in the ICRP model are based on
the available experimental data for humans, baboons and dogs and data for chronic exposuresof humans. Liver compartments called Liver 1 and Liver 2 are used to model the short-term
retention of uranium shown by the experimental data and the long-term retention indicated by
the environmental data. It is assumed that 1.5% of uranium leaving the circulation deposits in
Liver 1 and that the retention half-time for this compartment is 7 days. Outflow from Liver 1
is divided between Liver 2 and plasma in the ration 7 : 93 The half-time of retention in Liver
2 is assumed to be 10 years.

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DRAFT FOR MC REVIEW PRIOR TO CONSULTATION

12369
12370
12371
12372
12373
12374
12375
12376
12377
12378
12379
12380
12381
12382
12383
12384
12385
12386
12387
12388
12389
12390
12391
12392
12393
12394
12395
12396
12397
12398
12399

Figure 15-4. Observations and model predictions of cumulative urinary uranium in humansubjects as a function of time after intravenous injection with uranium isotopes (Leggett, 1994).
The three study groups indicated in the legend are described in the text.
Other soft tissues(965) The high initial uptake of uranium by soft tissues is discussed above. This ismodeled by assuming that 30% of outflow from plasma enters the soft-tissue compartment
ST0. Soft-tissue compartments called ST1 and ST2 are used to model intermediate and longterm retention of uranium in soft tissues. Parameter values for these compartments were set
for consistency with data for the Boston subjects and data for chronic exposure suggestingthat there may be significant long-term retention of uranium in soft tissues (Igarashi et al.,
1985; Fisenne et al., 1988; Gonzales and McInroy, 1991). For example, post-mortem data for
two non-occupationally exposed persons indicate that muscle and skin accounted for about
25% of retained uranium, with 70% in the skeleton (Gonzales and McInroy, 1991).
(966) Compartments ST1 and ST2 are assumed to receive 6.65% and 0.3%, respectively,of uranium leaving the circulation. Removal half-times from these compartments to plasma
are assumed to be 20 days and 100 years respectively. The model predicts that chronic soft
tissues (ST0+ST1+ST2) contain about 20% of total body uranium in chronically exposed
adults.
Retention in the skeleton(967) There is evidence that UO2++ exchanges with Ca++ at the surfaces of bone mineralcrystals, although UO2++ apparently does not participate in crystal formation or enter existing
crystals. Also, the early gross distribution of uranium in the skeleton is similar to that of
calcium. Like calcium, uranium is initially present on all bone surfaces but is mostconcentrated in areas of growth. Studies on dogs demonstrated that uranium on bone surfaces
diffuses into bone volume, although at a slower rate than calcium (Rowland and Farnham,
1969; Stevens et al., 1980). Such diffusion was absent or less pronounced in rodents (Priest
et al., 1982; Kisieleski et al., 1952). Autoradiographic studies of 233U in mice at 1 d and 224 dafter injection indicate an initial deposition of uranium on bone surfaces and subsequent311

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12400
12401
12402
12403
12404
12405
12406
12407
12408
12409
12410
12411
12412
12413
12414
12415
12416
12417
12418
12419
12420
12421
12422
12423
12424
12425
12426
12427
12428
12429
12430
12431
12432
12433
12434
12435
12436
12437
12438
12439
12440
12441
12442
12443
12444
12445
12446
12447

burial of lines of activity as well as some evidence of diffuse activity within bone mineral(Ellender et al., 1995). In all species for which there are data, there is evidence of similarity tocalcium in that return of uranium from bone to plasma occurs at rates that are greater than
could be attributed only to bone resorption.
(968) Parameter values for uptake and retention in the skeleton were based on data fromthe Boston study, animal data, post-mortem measurements on environmentally andoccupationally exposed humans, analogy with the alkaline earth elements and considerationsof bone metabolism. Each of the data sets has important limitations to their usefulness for theprediction of the skeletal kinetics of uranium in healthy humans. The Boston subjects were
terminally ill, and their calcium metabolism cannot reliably be regarded as normal.
Extrapolation of biokinetic data from laboratory animals to man is prone to error, particularly
data for rodents. Baboon data for uranium are limited, and the dog data are subject touncertainties resulting from the use of high masses of uranium, small number of animals andsmall bone samples. Some investigators have reported much higher early accumulation of
uranium in the skeleton than assumed in the model. For example, Sanotskii et al. (1963,1964) reported high initial deposition of uranium in the skeleton (25-40% of the administeredamount) in dogs, rabbits and rats after subcutaneous or intratracheal administration of uranyl
nitrate, although only 3-4% was retained after 6 months.
(969) It is assumed in the model that 15% of uranium leaving the circulation deposits onbone surfaces. By analogy with the alkaline earth elements (ICRP, 1993), the ratio of theamount deposited on trabecular surfaces to that deposited on cortical surfaces is assumed tobe 1.25 in the mature skeleton (after 25 years of age). The value of 1.25 is derived from anaverage six-fold greater rate of turnover of trabecular bone divided by a four-fold greater
cortical bone mass (Leggett et al., 1982; Leggett, 1992). The rate of removal of uranium frombone surfaces cannot be estimated with much certainty, but reasonable lower and upperbounds can be determined. Uranium apparently leaves bone surfaces much more slowly thancalcium (Rowland and Farnham, 1969; Stevens et al., 1980), but a half-time longer than about
5 – 10 days would be difficult to reconcile with the relatively rapid loss of uranium from boneseen in human and most animal studies. The assumption made is of a removal half-time of 5days, compared with a value of 1 day for calcium (Leggett, 1992). Because of recycling, theapparent retention time on bone surfaces will be greater than 5 days. For consistency with theavailable experimental data for the first few weeks after injection, it is assumed that 50% of
uranium from bone surfaces returns to plasma and 50% transfers to exchangeable bonevolume.
(970) The removal half-time assigned to the exchangeable bone volume is 30 days. Thisvalue was derived for radium and lead (Leggett, 1992, 1993). From exchangeable bonevolume, 75% of uranium is returned to bone surfaces and 25% transfers to non-exchangeablebone volume. Removal from non-exchangeable bone volume to plasma is assumed to occur
at the rate of bone turnover (reference values given in ICRP, 2002).
(971) The model predicts that the uranium content of the skeleton is about 30 times greaterthan that of the liver following constant chronic exposures to uranium, in reasonableagreement with most autopsy data for occupational or environmentally exposed subjects. The
model predicts that the adult skeleton contains about 75% of the body content of uranium
after chronic exposure, consistent with autopsy data (Gonzales and McInroy, 1991).
15.3.3. Treatment of radioactive progeny(972) The dosimetrically significant progeny of uranium isotopes addressed in this report
312

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
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12449
12450
12451
12452
12453
12454
12455
12456
12457
12458
12459
12460
12461
12462
12463
12464
12465
12466
12467
12468
12469
12470
12471

are isotopes of actinium, thorium, protactinium, uranium, neptunium, plutonium, radium,radon, polonium, lead, bismuth, thallium, actinium, francium, or astatine. The models for
actinium, thorium, radium, radon, polonium, lead, bismuth, thallium, actinium, francium, andastatine produced in systemic compartments by serial decay of members of a uranium chain
are essentially the same as the models applied to these elements as progeny of radium (see thesection on radium). Uranium produced in a systemic compartment by serial decay of membersof a uranium chain is assigned the characteristic model for uranium. The characteristic
models for neptunium and plutonium applied in this series of reports are applied toneptunium and plutonium, respectively, produced in systemic compartments following intake
of a uranium parent. Protactinium produced in a systemic compartment following intake of auranium parent is assigned the characteristic model for thorium. Protactinium, neptunium, or
plutonium produced in a compartment that is not identifiable with a compartment in its modelis assumed to transfer to the central blood compartment at the rate 1000 d-1 if produced in a
blood compartment and at the rate of bone turnover if produced in an exchangeable bonevolume compartment.
15.4.

Individual monitoring

234

U(973) 234U intakes are determined by measuring the nuclide concentration in urine andfaeces. As 234U is a nuclide naturally present in the environment and in the diet, excretion
rates of natural uranium are expected and should be evaluated for the population in the regionof residence of the workers.
Isotope
234

U
U

234

12472
12473
12474
12475
12476
12477
12478

MethodofMeasurement
α spectrometry
α spectrometry

Typical
Detection Limit
0.3 mBq/L
1 mBq/24h

Achievabledetection limit
0.05 mBq/L
0.2 mBq/24h

235U(974) Measurements of 235U concentrations in urine and faeces are used to determine
intakes of the nuclide. The main techniques used for urinalysis are alpha spectrometry and
ICP-MS. 235U may also be monitored by in vivo lung counting. Whole Body Counting might
be used as a complement.
IsotopeMonitoring
Technique

Methodof Typical
Measurement
Detection Limit

Achievabledetection limit

235

Urine Bioassay
Urine Bioassay

α spectrometry
ICPM/S

0.3 mBq/L
0.001
µg/L
(0.016 mBq/L)
1 mBq/24h
8 Bq

0.05 mBq/L
8 E-07Bq/L
0.2 mBq/24h
3 Bq

60 Bq

40 Bq

U
U

235

235

U
U

235

235

U

12479
12480
12481

Monitoring
TechniqueUrine Bioassay
Faeces Bioassay

α spectrometry
γ-ray
spectrometry
Body γ-ray
spectrometry

Faeces Bioassay
Lung Counting
Whole
Counting

238U(975) Measurements of 238U concentrations in urine and faeces are used to determine

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12486
12487
12488

intakes of the nuclide. Several techniques are used for urine bioassays, alpha spectrometry,
ICP-MS, kinetic phosphorescence analysis (TrKPA) and fluorimetry. As 238 U is a nuclide
naturally present in the environment and in the diet, excretion rates of natural uranium are
expected and should be evaluated for the local population. 238U may also be monitored by invivo lung counting. 238 U detection is based on the 62.8 and 92.3 keV photons emitted by its
decay product 234Th.
IsotopeMonitoring
Technique

238

Urine Bioassay
Urine Bioassay

U
U

238

238

U
U
238
U
238
U
238

12489
12490
12491
12492
12493
12494
12495
12496
12497
12498
12499
12500
12501
12502
12503
12504
12505
12506
12507
12508
12509
12510
12511
12512
12513
12514
12515
12516
12517
12518
12519
12520

Urine Bioassay
Urine Bioassay
Faeces Bioassay
Lung Counting

Methodof Typical
Measurement
DetectionLimit
α spectrometry
0.3 mBq/L
ICPM/S
0.0015µg/L(0.03 mBq/L)
TrKPA
0.1µg/L
Fluorimetry
1 µg/L
α spectrometry
2 mBq/24h
γ-ray
50 Bq of Thspectrometry of 234
234
Th

Achievabledetection limit
0.05 mBq/L
0.002mBq/L
0.06 µg/L
0.2 mBq/24h
30 Bq of Th-234

References
André, S., Métivier, H., Auget, D., Lantenois, G., Boyer, M., Masse, R., 1989. Lung dissolution of
uranium tetrafluoride in rats and baboons. Comparison with dissolution by alveolar
macrophages in culture and chemical dissolution. Hum. Toxicol. 8, 111-119.
Ansoborlo, E, Chalabreysse, J., Escallon, S., Hengé-Napoli, M.H., 1990. In vitro solubility ofuranium tetrafluoride with oxidizing medium compared with in vivo solubility in rats. Int. J.
Radiat. Biol. 58, 681-689.
Ansoborlo, E., Chazel, V., Hengé_Napoli, M.H., Pihet, P., Rannou, A., Bailey, M.R., Stradling, N.,
2002. Determination of the physical and chemical properties, biokinetics, and dosecoefficients of uranium compounds handled during nuclear fuel fabrication in France.
Health Phys. 82(3), 279-289,
Ansoborlo, E., Chazel, V., Houpert, P., Hengé-Napoli, M.H., Paquet, F., Hodgson, A., Stradling, N.,
1998a. Assessment of physico-chemical and biokinetic properties of uranium peroxide
hydrate UO4. Health Phys., 75(4), 389-397
Ansoborlo, E., Hodgson, A., Stradling, G.N., Hodgson, S., Metivier, H., Hengé-Napoli, M.H., Jarvis,N., Birchall, A., 1998b. Exposure implications for uranium aerosols formed at a new laser
enrichment facility: application of the ICRP respiratory tract and systemic model. Radiat.
Prot. Dosim., 79(1-4), 23-27.
Ansoborlo, E., Prat, O., Moisy, P., Denauwer, C., Guilbaud, P., Carriere, M., Gouget B.,Duffield, J.,
Doizi D., Vercouter, T., Moulin, C., Moulin, V., 2006. Actinide in speciation in relation tobiological processes. Biochimie 88(11), 1605-18.
Bailey, M., Davis, K., 2002. Estimations of kidney uranium concentrations from published reports ofuranium intakes in man where subsequent effects on kidney function were monitored.
Annexe A to The Health Hazards of Depleted Uranium Munitions Part II. The Royal
Society, London. www.royalsoc.ac.uk/du..
Ballou, J.E., Gies, R.A., Case, A.C., Haggard, D.L., Bushbom, R.L., Ryan, J.L., 1986. Deposition andearly disposition of inhaled 233UO2(NO3)2 and 232UO2(NO3)2 in the rat. Health Phys. 51
755-771.
Barber, J.M. Forrest, R.D., 1995. A study of uranium lung clearance at a uranium processing plant.
Health Phys. 68 661-669.

314

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12521
12522
12523
12524
12525
12526
12527
12528
12529
12530
12531
12532
12533
12534
12535
12536
12537
12538
12539
12540
12541
12542
12543
12544
12545
12546
12547
12548
12549
12550
12551
12552
12553
12554
12555
12556
12557
12558
12559
12560
12561
12562
12563
12564
12565
12566
12567
12568
12569
12570

Bassett, S.H., Frankel, A., Cedars, N., VanAlstine, H., Waterhouse, C., Cusson, K., 1948. The
excretion of hexavalent uranium following intravenous administration.: II. Studies onhuman subjects. Rochester, New York, UR-37.
Beau, P.G., Chalabreysse, J., 1989. Knowledge gained from bioassay data on some metabolic andtoxicological features of uranium hexafluoride and its degradation products. Radiat. Prot.
Dosim. 26, 107-112.
Bečková, V., Malátová, I., 2008. Dissolution behaviour of 238U, 234U and 230Th deposited on filtersfrom personal dosemeters. Radiat. Prot. Dosim. 129(4): 469-472, published ahead of print
November 1, 2007 doi:10.1093/rpd/ncm455.
Begichev, S.N., Borovoj, A.A., Burlakov, E.V., Gagarinski, A., Ju Demin, V.F., Khodakovsky, I.L.,
Khrulev, A.A., 1989. Radioactive releases due to the Chernobyl accident. Int. Sem. “Fission
Product Transport Processes in Reactor Accidents”, May 22-26, 1989, Dubrovnik,
Yugoslavia.
Bernard, S.R., Struxness, E.G., 1957. A study of the distribution and excretion of uranium in man. An
Interim Report. Tennessee, USA, ORNL 2304.
Bernard, S.R., Muir, J.R., Royster, G.W., 1957. The distribution and excretion of uranium in man. In:
Proceedings of the Health Physics Society First Annual Meeting pp. 33-48.
Bhattacharyya, M.H., Larsen, R.P., Cohen, N., Ralston, L.G., Moretti, E.S., Oldham, R.D.. Ayres, L.,1989. Gastrointestinal absorption of plutonium and uranium in fed and fasted adult baboons
and mice: application to humans. Radiat. Prot. Dosim. 26, 159-165.
Boback, M.W., 1975. A review of uranium excretion and clinical urinalysis data in accidental
exposure cases. In: Proceedings of the Conference on Occupational Health Experience with
Uranium, pp. 226–243. Arlington Virginia, April 28–30, 1975, ERDA 93, US Energy
Research and Development Administration.
Bruenger, F.W., Atherton, D.R., Bates, D.S., Buster, D.S., Stevens, W., 1976. The early distribution
and excretion of 233U in the Beagle . University of Utah College of Medicine, Salt Lake
City, Report No. COO-119-251, pp. 194-202.
Campbell, E.E., McInroy, J.F., Schulte, H.F., 1975. Uranium in the tissue of occupationally exposed
workers. Conference on Occupational Health Experience with Uranium. Arlington VA, US
ERDA 93, 324-350.
Chalabreysse, J., Beau, P.G., Chevalier, C., Jeanmaire, L., Bataller, G., Bérard, P., Gibert, B., 1989.
French experience with uranium compounds. Radiat. Prot. Dosim. 26, 49-56.
Chazel, V., Gerasimo, P., Dabouis V., Laroche, P., Paquet, F., 2003. Characterisation and dissolutionof depleted uranium aerosols produced during impacts of kinetic energy penetrators against
a tank. Radiat. Prot. Dosim. 105(1-4) 163-166.
Chazel, V., Houpert, P., Ansoborlo, E., 1998. Effect of U3O8 specific surface area on in vitro
dissolution, biokinetics, and dose coefficients. Radiat. Prot. Dosim. 79(1-4) 39-42.
Chazel, V., Houpert, P., Hengé-Napoli, M.H., Paquet, F., Ansoborlo, E., 2000a. Experimental
determination of the solubility of industrial UF4 particles. Radiat. Prot. Dosim. 92(4) 289294
Chazel,V., Houpert, P., Ansoborlo, E., Hengé-Napoli, M.H., Paquet, F., 2000b. Variation ofsolubility, biokinetics and dose coefficients of industrial uranium oxides according to
specific surface area. Radiat. Prot. Dosim. 88(3) 223-231.
Cooke, N., Holt, F.B., 1974. The solubility of some uranium compounds in simulated lung fluid.
Health Phys. 27, 69-77.
Coombs M.A., Cuddihy R.G. 1983. Emanation of 232U daughter products from submicron particles
of uranium dioxide and thorium dioxide by nuclear recoil and inert gas diffusion. J. Aerosol
Sci. 14, 75-86.
Cooper, J.R., Stradling, G.N., Smith, H., Ham, S.E., 1982. The behaviour of uranium-233 oxide anduranyl-233 nitrate in rats. Int. J. Radiat. Biol. 41(4) 421-433.

315

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12571
12572
12573
12574
12575
12576
12577
12578
12579
12580
12581
12582
12583
12584
12585
12586
12587
12588
12589
12590
12591
12592
12593
12594
12595
12596
12597
12598
12599
12600
12601
12602
12603
12604
12605
12606
12607
12608
12609
12610
12611
12612
12613
12614
12615
12616
12617
12618
12619
12620
12621
12622

Cross, F. T., Palmer, R. F., Filipy, R. E., Dagle, G. E., Stuart, B. O., 1982, Carcinogenic effects ofradon daughters, uranium ore dust and cigarette smoke in beagle dogs. Health Phys. 42(1),33-52.
Cuddihy, R.G., Finch, G.L., Newton, G.J., Hahn, F.F. Mewhinney, J.A. Rothenberg, S.J., Powers,
D.A., 1989. Characteristics of radioactive particles released from the Chernobyl nuclear
reactor. Environ. Sci. Technol. 23, 89-95.
Devell, L., 1988. Nuclide composition of Chernobyl hot particles. In: von Phillipsborn, H.,
Steinhäusler F., (Eds.), Hot Particles from the Chernobyl Fallout. Proc. Int. Workshop,
Theuern, October 1987, pp. 23-34. Bergbau und Industriemuseum Ostbayern, Band 16.
Donoghue, J.K., Dyson, E.D., Hislop, J.S., Leach, A.M., Spoor, N.L., 1972. Human exposure tonatural uranium. Brit. J. Indust. Med. 29, 81-89.
Duport, P., Robertson, R., Ho, K., Horvath, F., 1991.) Flow-through dissolution of uranium-thorium
ore dust, uranium concentrate, uranium dioxide, and thorium alloy in simulated lung fluid.
Radiat. Prot. Dosim. 38(1/3) 121-133.
Durbin, P.W., 1984. Metabolic models for uranium. In Proceedings of a colloquium: Biokinetics andanalysis of uranium in man. 8-9 Aug. 1984 (Moore RH Ed). Richland, USA, United States
Uranium Registry/Hanford Environmental Health Foundation. USUR-05 HEHF-47,
Document No:PB86-203080, F1-F65.
Eidson, A.F., 1990. Biological characterisation of radiation exposure and dose estimates for inhaleduranium mining effluents
NUREG/CR-5489 TI90 012914, United States Nuclear
Regulatory Commission.
Eidson, A.F., 1994. The effect of solubility on inhaled uranium compound clearance: a review.
Health Phys. 67, 1-14.
Elder, J.C., Tinkle, M.C., 1980. Oxidation of Depleted Uranium Penetrators and Aerosol Dispersal atHigh Temperatures. Los Alamos National Laboratory Report LA-8610-MS. http://libwww.lanl.gov/la-pubs/00313603.pdf
Ellender, M., Haines, J.W., Harrison, J.D., 1995. The distribution and retention of plutonium,
americium and uranium in CBA/H mice. Hum. Exper. Toxicol. 14, 38-48.
Ellender, M., 1987. The clearance of uranium after deposition of the nitrate and bicarbonate in two
regions of the rat lung. Human Toxicol. 6, 479-482.
Fisenne, I.M., Welford, G.A., 1986. Natural U concentrations in soft tissues and bone of New York
City residents. Health Phys. 50(6) 739-46.
Fisenne, I.M., Perry, P.M., Harley, N.H., 1988. Uranium in humans. Radiat. Prot. Dosimetry 24(1/4)
127-131.
Fish, B.R., Bernard, S.R., 1961. Unpublished data. Sixth Conference on Industrial Hygiene and Air
Pollution and summarized in Industrial Hygiene News Reports IV 1.
Fisher, D.R., Jackson, P.O., Brodaczynski, G.G., Scherpelz, R.I., 1983. Levels of 234U, 238U and 230Th
in excreta of uranium mill crushermen. Health Phys. 45, 617-629.
Fisher, D.R, Swint, M.J., Kathren, R.L., 1991. Modified biokinetic model for uranium from analysisof acute exposure to UF6. Health Phys. 60, 335-342.
Fisher, D.R., Briant, J.K., 1994. Assessment of accidental intakes of uranyl acetylacetonate (UAA).
Radiat. Prot. Dosim. 53(1-4) 263-267.
Glissmeyer, J.A., Mishima, J., 1979. Characterization of Airborne Uranium from Test Firings of
XM774 Ammunition. Pacific Northwest Laboratory. PNL-2944. Richland, WA.
Gonzales, E.R., McInroy, J.F., 1991. Abstract WPM-A1: The distribution of uranium in two wholebodies. Health Phys. 60[Supplement 2], S51.
Griffith W.C., Cuddihy R.G., Hoover M.D. Stalnaker N.D., 1980. Simulation of the retention anddosimetry of 232U and its daughters after inhalation in ThO2 or UO2 particles. In: Sanders,
C.L., Cross, F.T., Dagle, G.E., Mahaffey, J.A., (Eds.), Pulmonary Toxicology of Respirable
Particles. pp. 193-208 Proc. 19th Annual Hanford Life Sciences Symposium at Richland,
WA. CONF-791002. Available from National Technical Information Service. Springfield.
Virginia.

316

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12623
12624
12625
12626
12627
12628
12629
12630
12631
12632
12633
12634
12635
12636
12637
12638
12639
12640
12641
12642
12643
12644
12645
12646
12647
12648
12649
12650
12651
12652
12653
12654
12655
12656
12657
12658
12659
12660
12661
12662
12663
12664
12665
12666
12667
12668
12669
12670
12671
12672
12673
12674

Guilmette, R.A., Cheng, Y.S., 2009. Physicochemical characterization of Capstone depleted uranium
aerosols IV: in vitro solubility analysis. Health Phys. 96, 292-305.
Harduin, J.C., Royer, Ph., Piechowski, J., 1994. Uptake and urinary excretion of uranium after oral
administration in man. Radiat. Prot. Dosim. 53, 245-248.
Harris, W.B., 1961. Experimental clearance of uranium dust from the human body. In: Davies, C.N.,(Ed.), Inhaled Particles and Vapours. Proc. of an International Symposium organised by the
British Occupational Hygiene Society. Oxford, Pergamon Press, pp. 209-220.
Harrison, J.D., 1991. The gastrointestinal absorption of the actinide elements. Sci. Total Environment
100, 43-60.
Hill, C. R., 1962, Identification of alpha emitters in normal biological material. Health Phys. 8, 17–25.
Hodgson, A., Moody, J.C., Stradling, G.N., Bailey, M.R., Birchall, A., 2000. Application of the ICRP
respiratory tract model to uranium compounds produced during the manufacture of nuclear
fuel. NRPB-M1156, Chilton.
Hursh, J.B., Spoor, N.L., 1973. Data on Man. In: Hodge, H.C., Stannard, J.N., Hursh, J.B., (Eds.),
Uranium, plutonium, transplutonic elements. Handbook of Experimental Pharmacology 36.
New York. Springer-Verlag, pp. 197-239.
Hursh, J.B., Neuman, W.R., Toribara, T., Wilson, H., Waterhouse, C., 1969. Oral ingestion of
uranium by man. Health Phys. 17, 619-621.
ICRP, 1979. Limits for Intakes of Radionuclides by Workers. ICRP Publication 30 Part 1. Ann.
ICRP 2(3/4).
ICRP, 1993. Age-dependent Dose to Members of the Public from Intake of Radionuclides. Part 2.
ICRP Publication 67. Ann. ICRP 23(3/4).
ICRP, 1994a. Dose Coefficients for Intakes of Radionuclides by Workers. ICRP Publication 68, Ann
ICRP, 24(4), 12.
ICRP, 1994b. Human Respiratory Tract Model for Radiological Protection. ICRP Publication 66.
Ann. ICRP 24(1/3).
ICRP, 1995. Age-dependent Doses to Members of the Public from Intake of Radionuclides. Pt.3.
ICRP Publication 69. Ann. ICRP 25(1).
ICRP, 1997. Individual monitoring for internal exposure of workers. ICRP Publication 78. Ann. ICRP
27(3-4).
ICRP, 2002. Guide for the Practical Application of the ICRP Human Respiratory Tract Model.
Supporting Guidance 3. Ann. ICRP, 32(1-2).
Igarashi, Y., Yamakawa, A., Seki, R., Ikeda, N., 1985. Determination of U in Japanese human tissues
by the fission track method. Health Physics 49, 707-712.
Jones, E.S., 1966. Microscopic and autoradiographic studies of distribution of uranium in the rat
kidney. Health Physics 12, (10) 1437-51.
Kathren, R.L., McInroy, J.F., Moore, R.H., Dietert, S.E., 1989. Uranium in the tissues of an
occupationally exposed individual. Health Phys. 57, 17-21.
Kisieleski, W.E., Faraghan, W.G., Norris, W.P., Arnold, J.S., 1952. The metabolism of uranium-233
in mice. J. Pharm. Exper. Therapeutics 104(4) 459-67.
Larsen, R.P., Orlandini, K.A., 1984. Gastrointestinal absorption of uranium in man. In:
Environmental Research Division Annual Report, July 1982 - June 1983; Argonne National
Laboratory, ANL-83-100-Pt.2. pp.46-50.
Leach, L.J., Yuile, C.L., Hodge, H.C., Sylvester, G.E., Wilson, H.B., 1973. A five-year inhalation
study with natural uranium dioxide (UO2) dust—II. Post-exposure retention and biologic
effects in the monkey, dog and rat. Health Phys. 25, 239-258.
Leggett, R.W., 1989. The behavior and chemical toxicity of U in the kidney: a reassessment. HealthPhys., 57(3) 365-83.
Leggett, R.W., 1992. A generic age-specific biokinetic model for calcium-like elements. Radiation
Protection Dosimetry 41, 183-198.
Leggett, R.W., 1993. An age-specific kinetic model of lead metabolism in humans. Environmental

317

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12675
12676
12677
12678
12679
12680
12681
12682
12683
12684
12685
12686
12687
12688
12689
12690
12691
12692
12693
12694
12695
12696
12697
12698
12699
12700
12701
12702
12703
12704
12705
12706
12707
12708
12709
12710
12711
12712
12713
12714
12715
12716
12717
12718
12719
12720
12721
12722
12723
12724
12725
12726

Health Perspectives 101(7) 598-616.
Leggett, R.W., 1994. Basis for the ICRP's age-specific biokinetic model for uranium. Health Phys.
67, 589-610.
Leggett, R.W., Pellmar, T.C., 2003. The biokinetics of uranium migrating from embedded DU
fragments. J Environ. Radioact. 64(2-3) 205-25.
Leggett, R.W., Eckerman, K.F., Williams, L.R., 1982. Strontium-90 in bone: A case study in agedependent dosimetric modelling. Health Phys. 43(3) 307-322.
Leggett, R.W., Eckermann, K.F., Boice, J.D., 2005. A respiratory model for uranium aluminide basedon occupational data. J. Radiol. Prot. 25, 405–416.
Leggett, R.W., 1994. Basis for the ICRP's age-specific biokinetic model for uranium. Health Phys.
67, 589-610.
Leggett, R.W., Harrison, J.D., 1995. Fractional absorption of ingested U in humans. Health Phys. 68,
1-15.
Lipsztein, J.L., 1981. An improved model for uranium metabolism in the primate. Ph.D Dissertation,
New York University.
Luessenhop, A.J., Gallimore, J.C., Sweet, W.H., Struxness, E.G., Robinson, J., 1958. The toxicity ofhexavalent uranium following intravenous administration. Am J. Roentgenol. 79, 83-100.
Marsh J.W., Gregoratto, D., Karcher, K., Nosske D., Bessa Y., Blanchardon E., Hofmann W.,
Tomasek L., 2011. Dosimetric calculations for uranium miners for epidemiological studies.
Radiat. Prot. Dos. pp. 1-13, doi:10.1093/rpd/ncr310.
Metivier, H., Poncy, J.L., Rateau, G., Stradling, G.N., Moody, J.C., Gray, S.A., 1992. Uranium
behaviour in the baboon after the deposition of a ceramic forms of uranium dioxide anduranium octoxide in the lungs: Implications for human exposure. Radioprot. 27, 263-281.
Mishima, J., Parkhurst M.A., Scherpels, R.L., Hadlock, D.E., 1985. Potential Behavior of Depleted
Uranium Penetrators under Shipping and Bulk Storage Accident Conditions. PacificNorthwest Laboratory. PNL-5415. Richland, WA.
Mitchell, R.E.J., Sunder, S., 2004. Depleted uranium dust from fired munitions: physical, chemicaland biological properties. Health Phys. 87(1) 57–67.
Moody, J.C., Birchall, A., Stradling, G.N., Britcher, A.R., Battersby, W., 1997. Biokinetics ofrecycled uranium trioxide and implications for human exposure. Inhaled Particles VIII.
Annals of Occupational Hygiene. 41 Suppl.1, 104-110.
Moore, R.H., Kathren, R.L., 1985. A World War II uranium hexafluoride inhalation event withpulmonary implications for today. J. Occup. Med. 27, 753–756.
Morrow, P., Gelein, R., Beiter, H., Scott, J.B., Picano, J.J., Yuile, C.L., 1982. Inhalation andintravenous studies of UF6/UO2F2 in dogs. Health Phys. 43(6) 859-874.
Morrow, P.E., Gibb, F.R., Beiter, H.D., 1972. Inhalation studies of uranium trioxide. Health Phys. 23,
273-280.
Muir, J.R., Fish, B.R., Jones, E.S., Gillum, N.L., Thompson, J.L., 1960. Distribution and excretion of
uranium. Oak Ridge, USA, Health Physics Division Annual Progress Report for period
ending July 31, 1960. Report No. ORNL-2994.
Neton, J., Lo Sasso, T., Lipsztein, J., Wrenn, M.E., Cohen, N., 1979. Short term kinetics of uranium
in the adult baboon : Preliminary data. Radioactivity studies progress report. COO-3382-18,
Institute of Environmental Medicine, New York University Medical Center.
OSAGWI, 2000. (Office of the Special Assistant to the Deputy Secretary of Defense for Gulf War
Illnesses. DoD) Exposure Investigation Report, Depleted Uranium in the Gulf (II),
December 2000 at www.gulflink.osd.mil in the Environmental Exposure Reports Section.
Parkhurst, M.A., Szrom, F., Guilmette, R.A., Holmes, T.D., Cheng, Y.S., Kenoyer, J.L., Collins,
J.W., Sanderson, T.E., Fliszar, R.W., Gold, K., Beckman, J.C., Long, J.A., 2004a. Capstone
Depleted Uranium Aerosols: Generation and Characterization, Volumes 1. Main Text.
Attachment 1 of Depleted Uranium Aerosol Doses and Risks: Summary of U.S.
Assessments. PNNL-14168, Prepared for the U.S. Army by Pacific Northwest National
Laboratory, Richland, Washington.

318

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12727
12728
12729
12730
12731
12732
12733
12734
12735
12736
12737
12738
12739
12740
12741
12742
12743
12744
12745
12746
12747
12748
12749
12750
12751
12752
12753
12754
12755
12756
12757
12758
12759
12760
12761
12762
12763
12764
12765
12766
12767
12768
12769
12770
12771
12772
12773
12774
12775
12776
12777
12778

Parkhurst, M.A., Szrom, F., Guilmette, R.A., Holmes, T.D., Cheng, Y.S., Kenoyer, J.L., Collins,
J.W., Sanderson, T.E., Fliszar, R.W., Gold, K., Beckman, J.C., Long, J.A., 2004b. Capstone
Depleted Uranium Aerosols: Generation and Characterization, Volume 2. Appendices.
Attachment 2 of Depleted Uranium Aerosol Doses and Risks: Summary of U.S.
Assessments. PNNL-14168, Prepared for the U.S. Army by Pacific Northwest National
Laboratory, Richland, Washington.
Parkhurst, M.A., Guilmette, R.A., 2009. Overview of the Capstone depleted uranium study ofaerosols from impact with armored vehicles: Test setup and aerosol generation,
characterization, and application in assessing dose and risk. Health Phys. 96, 207-220.
Pellow, P.G., Stradling, G.N., Hodgson, A., Fell, T.P., Phipps, A. Ellender, M., 1996. Biokinetics ofUranium Tributyl Phosphate in the Rat : Implications for Occupational Exposure. NRPBM682, Chilton.
Pellow, P.G., Stradling, G.N., Hodgson, A., Fell, T.P., Phipps, A. and Ellender, M., 1997. Absorption
kinetics of uranium tri-n-butyl phosphate in the rat: Implications for occupational exposure.
Journal of Radioanalytical and Nuclear Chemistry 226, 93-98.
Pomroy, C., Noel, L., 1981. Retention of uranium thorax burdens in fuel fabricators. Health Phys. 41,
393-400.
Price, A., 1989. Review of methods for assessment of intake of uranium by workers at BNFL
Springfields. Radiat. Prot. Dosim. 26(1/4) 35-42.
Priest, N.D., Howells, G.R., Green, D. Haines, J.W., 1982. Uranium in bone: metabolic andautoradiographic studies in the rat. Human Toxicol. 1, 97-114.
Roberts, A.M., Coulston, D.J., Bates, T.H., 1977. Conformation of in vivo uranium-in chest survey
by analysis of autopsy specimens. Health Phys., 32(5) 435-7.
Rowland, R.E., Farnham, J.E., 1969. The deposition of uranium in bone. Health Phys. 17(1) 139-44.
Russell, J.J., Kathren, R.L., 2004. Uranium deposition and retention in a USTUR whole body case.
Health Phys. 86, 273-284.
Sanotskii, V.A., Mikhailovich, S.M., Ivannikov, A.T., 1963. Abstract No. 40513: The toxic effect ofuranium compounds. Nuclear Science Abstracts 17, 5450.
Sanotskii, V.A., Mikhailovich, S.M., Ivannikov, A.T., 1964. The toxic effect of uranium compounds.
In: Radiological Health and Safety in mining and milling of nuclear materials. Vienna,
IAEA pp. 275-288.
Saxby, W.N., Taylor, N.A., Garland, J., Rundo, J., and Newton, D., 1964. A Case of inhalation ofenriched uranium dust. In: Assessment of Radioactivity in Man, Volume II. Vienna, IAEA,
pp. 535-547.
Schieferdecker, H., Dilger, H., Doerfel, H., 1985. Inhalation of U aerosols from UO2 fuel element
fabrication. Health Phys. 48(1) 29-48.
Scripsick, R.C., Crist, K.C., Tillery, M.I., Soderholm, S.C., Rothenberg, S.J., 1985a. Preliminary
Study of Uranium Oxide Dissolution in Simulated Lung Fluid. LA-10268-MS, Los Alamos
National Laboratory. http://lib-www.lanl.gov/la-pubs/00318819.pdf.
Scripsick, R.C., Crist, K.C., Tillery, M.I., Soderholm, S.C., 1985b. Differences in in vitro dissolution
properties of settled and airborne uranium material. In: Stocker, H., (Ed.), Occupational
Radiation Safety in Mining Canadian Nuclear Association pp. 255-260. http://libwww.lanl.gov/la-pubs/00374828.pdf.
Singh, N. P., Wrenn, M. E., McInroy, J. F., Gonzales, E., Cross, F. T., Jackson, P. O. 1986a Ratios of234
U, 238U and 230Th in dogs' lungs exposed to uranium ore dust: An interlaboratorycomparison. Health Phys., 50, 292-297.
Singh, N.P., Bennett, D.D., Wrenn, M.E., Saccomanno, G., 1987. Concentrations of alpha-emitting
isotopes of U and Th in uranium miners' and millers' tissues. Health Phys. 53(3) 261-265.
Singh, N.P., Lewis, L.L., Wrenn, M.E., 1986b. Abstract THAM-E3: Uranium in human tissues ofColorado, Pennsylvania and Utah populations. Health Phys., 50, (Supplement 1) S83.
Sontag, W., 1984. Long-term behaviour of 239Pu, 241Am and 233U in different bones of one-year-old
rats: macrodistribution and macrodosimetry. Human Toxicol. 3, 469-483.

319

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12779
12780
12781
12782
12783
12784
12785
12786
12787
12788
12789
12790
12791
12792
12793
12794
12795
12796
12797
12798
12799
12800
12801
12802
12803
12804
12805
12806
12807
12808
12809
12810
12811
12812
12813
12814
12815
12816
12817
12818
12819
12820
12821
12822
12823
12824
12825
12826
12827
12828
12829
12830

Spencer, H., Osis, D., Fisenne, I.M., Perry, P.M., Harley, N.H., 1990. Measured intake and excretion
patterns of naturally occurring 234U, 238U and calcium in humans. Radiat. Res. 124, 90-95.
Stevens, W., Bruenger, F.W., Atherton, D.R., Smith, J.M., Taylor, G.N., 1980. The distribution andretention of hexavalent 233U in the Beagle. Radiat. Res., 83, 109-126.
Stradling, G.N., Stather, J.W., Gray, S.A., Moody, J.C., Ellender, M., Hodgson, A., Sedgwick D.,
Cooke, N., 1987. The metabolism of uranium in the rat after inhalation of two industrial
forms of ore concentrate: the implications for occupational exposure. Human Toxicol. 6,385-393.
Stradling, G.N., Stather, J.W., Price, A., Cooke, N., 1989. Limits on intake and the interpretation ofmonitoring data for workers exposed to industrial uranium bearing dusts. Radiat. Prot.
Dosim. 26(1/4). 83-87.
Stradling, G.N., Stather, J.W., Strong, J.C., Sumner, S.A., Moody, J.C., Towndrow, C.G., Hodgson,
A., Sedgwick, D., Cooke, N., 1988. The metabolism of ceramic and non-ceramic forms ofuranium dioxide after deposition in the rat lung. Human Toxicol. 7, 133 - 139.
Stradling, G.N., Stather, J.W., Strong, J.C., Sumner, S.A., Towndrow, C.G., Moody, J.C., Sedgwick,D., Cooke, N., 1985a. The metabolism of some industrial uranium tetrafluorides after
deposition in the rat lung. Human Toxicol. 4, 159-168.
Stradling, G.N., Stather, J.W., Ellender, M., Sumner, S.A., Moody, J.C., Towndrow, C.G., Hodgson,
A., Sedgewick, D., Cooke, N., 1985b. Metabolism of an industrial uranium trioxide dust
after deposition in the rat lung. Human Toxicol. 4, 563-572.
Stradling, N., Hodgson, A., Ansoborlo, E., Berard, P., Etherington, G., Fell, T., Rance, E., Le Guen,
B., 2002. Industrial uranium compounds: exposure limits, assessment of intake and toxicity
after inhalation NRPB-W22, Chilton.
Stradling, G.N., Gray, S.A., Moody, J.C., Ellender, M., Pearce, M., 2005. Biokinetics of thorium inthe presence of a highly transportable form of uranium: Implications for occupational
exposure. NRPB-DA/04/2005, Chilton.
Struxness, E.G., Luessenhop, A.J., Bernard, S.R., Gallimore, J.C., 1956. The distribution andexcretion of hexavalent uranium in man. IN Proceedings of the international conference on
the peaceful uses of atomic energy 8 Aug. 1955-20 Aug. 1955 New York, United Nations,186-196.
Stuart, B. O. Beasley, T. M., 1967, Non-equilibrium tissue distributions of uranium and thorium
following inhalation of uranium ore by rats. In: Davies, C. N., editor. Inhaled Particles andVapours II. Proceedings of an International Symposium organised by the British
Occupational Hygiene Society; Cambridge, UK. Oxford: Pergamon Press pp. 291-8.
Stuart, B.O., Jackson, P.O., 1975. The inhalation of uranium ores. In: Wrenn, M.E., (Ed.), Proc. of
the Conference on Occupational Health Experience with Uranium. Arlington, Virginia,
ERDA 93. US Energy Research and Development Administration, pp. 130–139. Available
from National Technical Information Service, Springfield, Virginia.
Sullivan, M.F., 1980. Absorption of actinide elements from the gastrointestinal tract of rats, guinea
pigs and dogs. Health Phys. 38, 159-171.
Tannenbaum, A., 1951. Toxicology of uranium: Survey and collected papers. New York, USA,
McGraw-Hill Book Company Inc. National Nuclear Energy Series, Manhattan ProjectTechnical Section.
Terepka, A.R., Toribara, T.Y., Neuman, W.F., 1964. Abstract 22: Skeletal retention of uranium inman. In: 46th meeting of the Endocrine Society 1964, p. 33.
Toivonen, H., Pöllämem, R., Leppänen, A., Klemola, S., Lathinen, J., 1992. Release from the nuclear
power plant in Sosnovyy Bor in March 1992. Radiochimica Acta 57, 169-172.
West, C.M., Scott, L., Schultz, N.B., 1979. Sixteen years of uranium personnel monitoring
experience. In retrospect. Health Phys. 36, 665-669.
Wood, S.K., Farnham, J.E., Marshall, J.H., 1970. 45Ca, 133Ba, and 226Ra in 6- to 10-year-old Beagle
dogs: a 100 day study. Argonne, Illinois, ANL-7760 Part II Biology and Medicine. July
1969-June 1970, pp. 110-132.

320

DRAFT FOR MC REVIEW PRIOR TO CONSULTATION
12831
12832
12833
12834
12835
12836
12837
12838
12839
12840
12841

Wrenn, M.E., Singh, N. P., Saccomanno, G., 1983. Uranium and thorium isotopes and their state ofequilibria in lungs from uranium miners. Health Phys. 44 Suppl. 1, 385-389.
Wrenn, M.E., Durbin, P.W., Howard, B., Lipzstein, J., Rundo, J., Still, E.T., Willis, D.L., 1985.
Metabolism of ingested U and Ra. Health Phys. 48, 601-603.
Wrenn, M.E., Singh, N.A., Ruth, H., Rallison, M.I., Burleigh, D.P., 1989. Gastrointestinal absorptionof soluble uranium from drinking water by man. Radiat. Prot. Dosim. 26, 119-122.
Zamora, L., Zielinski, J.M., Meyerhof, D.P., Tracy, B.L., 2002. Gastrointestinal absorption of
uranium in humans. Health Phys. 83(1) 35-45.
Zhao, S.L., Zhao, F.-Y., 1990. Nephrotoxic limit and annual limit of intake for natural U. Health
Phys; 58(5) 619-623.

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